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Alternative treatment of common skin disorders

Alternative treatment aims not only to minimize the patient's complaints, but also to restore the skin barrier function as quickly as possible in order to reduce the effects of irritants or allergens. 
Crusts should be first removed gently by a tepid water bath, preferably supplemented with anti-inflammatory agents (e.g., wheat bran) and bath oil, or by wet dressings. With efficient anti-inflammatory treatment itching also resolves in many cases. 

Most drugs used in dermatology are topical: they are applied to the skin surface in the form of ointments, creams, lotions, gels, and powders. 

Topical drugs have advantages over systemic drugs. They deliver the medication directly to the organ that needs treatment - sometimes called the target organ - the skin. Topicals are also less likely to provoke systemic side effects than systemic drugs are. 

A topical drug cannot be effective if it does not penetrate the skin's outer protective layer and deliver its healing medication. Penetration through the skin is affected by the condition of the skin itself and the physical and chemical properties of the two parts of a topical dermatologic drug: the active, the vehicle and the presence of skin enhancer. 
Topical herbal drugs can be an alternative for treating skin ailments if we take into consideration their benefit/risk ratio compared to synthetic drugs. Many of the well-known plants are currently widely accepted by patients because of their heeling power. The efficacy of herbal drugs, their extracts and isolated substances can be deduced from pharmacological and biochemical in vitro experiments. Clinical trials are very promising (24).


Dermatitis is a complex clinical picture that must be comprehended not merely as skin disease, but rather as disturbances of the entire organism. An alternative to academic medical treatments is therapy with natural remedies, in view of the fact that they act upon the pathological process of the diseases in accordance with the particular drug-symptom complexes involved (25). 

The skin healing formulations of Multipurpose Phytocort Cream is optimized in terms of macroscopic characteristics including spreadability, penetrability, and lipidity. Some of the ingredients are fat-soluble while others are more hydrophilic. In order for All Purpose Phytocort dermal preparation to contain the whole complex of the drug constituents, oil in water emulsion have been prepared, in which both phases of the emulsion system are enriched by the pertinent lipophilic and hydrophilic ingredients and mixed together in a latter step. A modification of the composition and a selection of the emulsifier can modify the structure, type of cream, as well as its viscosity from the aspect of achieving optimal application and effect (26). Thus the optimized formulation, which is emulsion of oil in water, results in enhanced diffusion of active ingredients. 

The ointment is usually soft, white, non-greasy, and it vanish when rubbed into the skin. Ointment is a versatile vehicle that is useful in a wide range of skin diseases. They are easy to rub in and do not feel tacky or greasy.


1. Modulates the immune system.
2. Exhibits anti-inflammatory action.
3. Inhibits the release of proinflammatory cytokines.
4. Increases the epidermal lipids.
5. Exhibits moisturizing effect and maintain normal transepidermal water loss.
6. Exhibits antibacterial, antiviral and antifungal effect.
7. Increases the resistance of blood vessels.
8. Exhibits Antioxidant activity (oxygen and nitrous oxide free radicals scavenger).
9. Relieves the pruritis.
10. Modulate fibroblast hyperproliferation during epithelial regeneration.



Tea tree oil has been found to be useful in removing transient skin flora while suppressing but maintaining normal resident flora (27). 

Terpinen-4-ol, alpha-Terpineol and Alpha-pinene are the active constituents in tea tree oil. They were found to be active against Propionibacterium acnes, Staphylococcus aureus, and Staph. Epidermidis (28). Studies showed that 32 strains of Propionibacterium acnes are susceptible to the essential oil of Melaleuca alternifolia, tea tree oil. The minimum bactericidal concentration of tea tree oil for five strains was 0.25% or less while, for the remainder, it was 0.50% (29). Isolates of Staphylococcus aureus tested were susceptible to the Tea tree essential oil. Of the isolates tested, 64 were methicillin-resistant S. aureus and 33 were mupirocin-resistant (30).
The in vitro antifungal activity of tea oil, the essential oil of Melaleuca alternifolia, has been evaluated against 26 strains of various dermatophyte species, 54 yeast, among them 32 strains of Candida albicans and other Candida sp. as well as 22 different Malassezia furfur strains. Tea tree oil was found to be able to inhibit growth of all clinical fungal isolates (31).
Randomized clinical trial has been performed on 124 patients to evaluate the efficacy and skin tolerance of 5% tea-tree oil in the treatment of mild to moderate acne, and compared with 5% benzoyl peroxide lotion. The results of this study showed that both 5% tea-tree oil 5% benzoyl peroxide had a significant effect in ameliorating the patients' acne by reducing the number of inflamed and non-inflamed lesions (open and closed comedones) although the onset of action in the case of tea-tree oil was slower. Encouragingly, fewer side effects were experienced by patients treated with tea-tree oil (32). 

BORAGE OIL (A Source of Polyunsaturated fatty acids)
The skin epidermis displays a highly active metabolism of polyunsaturated fatty acids. Deficiency of Linoleic acid and gamma lenolenic acid precursors of arachidonic acid results in characteristic scaly skin disorder and excessive epidermal water loss. Arachidonic acid is metabolized into prostaglandins. It has been found that prostaglandins modulate normal skin physiological processes at low concentrations and inflammatory reactions at high concentration. Thus, appropriate supplementation with purified vegetable oils rich in arachidonic acid precursors may generate local cutaneous anti-inflammatory metabolites which could serve as a less toxic in vivo monotherpy or as adjuncts to standard therapeutic regimens for the management of skin inflammatory disorders (33). 

Experimental studies showed that arachidonic acid precursor fatty acids are effectively incorporated into the cellular lipid of human keratinocytes (34). Fatty acids have been studied in the hyperkeratotic stratum corneum. The results showed a defect in the maturation of fatty acids. This presents evidence that the abnormality of lipid metabolism can influence the process of desquamation in stratum corneum (35). 

Using Borage oil rich in GLA has shown to correct deficiencies in skin lipids in subgroup of patients with atopic dermatitis with clinical improvement of the symptoms (36). Topically applied fatty acid has been found to be able to penetrate to the living cells of normal epidermis, enter into metabolism and significantly modify endogenous epidermal lipids (37). 

As it has been proven by studies that gamma-Linolenic acid (GLA), a precursor of arachidonic acid, possesses physiological functions of modulating immune and inflammatory response, various techniques are employed for the enrichment and purification of GLA in borage oil. Highly purified GLA is desired both as a medicine and as an ingredient of cosmetics (38). 

Borage oil is a rich source of Essential Fatty Acids that play a fundamental role in all cell membranes of the body, and they are vital for metabolism. The fluidity and flexibility of cell membranes depend on the amount of essential Fatty Acids they have. They are also the precursors of the important short-lived regulating molecules, the prostaglandins (39). 

In a clinical study of infantile seborrheic dermatitis, daily topical application of borage oil containing 24% GLA has been studied. It has been suggested that GLA is of importance in maintaining normal transepidermal water loss (40). 

The anti-inflammatory effect of GLA-fortified borage oil is due to the modulation of polymorphonuclear-neutrophils generation of proinflammatory leukotriene B-4 (41). 

Borage oil rich in gamma linolenic acid has been tested in animals and found to induce epidermal generation of local anti-inflammatory metabolites that have leukotriene inhibition potentials. It has been concluded that it has ameliorative effects on chronic inflammatory skin disorders (42). 

Borage oil, being a rich source of arachidonic acid -derived eicosanoid is considered potent modulators of hyperproliferation and inflammation of the skin (43). 

Studies showed that Arachidonic acid and linoleic acid mediate their ability to modulate inflammation and epidermal proliferation by being incorporated into epidermal phospholipids (44). 

Modern life stress leads to persistent activation of the neuroendocrine stress axis, which causes:

Increased release of oxygen free radicals.
Increased release of Nitrous oxide radicals.
Increased release of pro-inflammatory cytokines. 


For the correction of these metabolic states, an adequate supply of plant-based antioxidants, especially flavonoids are indicated. These are plant-based polyphenols, which like vitamins cannot be synthesized by the body. Vitamin E in combination with vitamin C and beta-carotene are currently considered worldwide as the standard antioxidative therapy. For a more reliable antioxidative action, adding a mixture of flavonoids seems preferable (45).

Flavonoids continue to attract wide attention as possible very useful agents for combating free radical pathologies, i.e. the pathological states associated with free radical overproduction (46). Experimental studies showed that Flavonoids, particularly quercetin, the most abundant flavonoid in plants has cytoprotective potential as they are likely to be important in defending human DNA against oxidative attacks (47). Experimental studies have also shown that flavonoids have protective effect on the skin against carcinogenic agents (48). 

Flavonoids relieves stress through its clear anxiolytic effect and thus stops the activation of the neuroendocrine stress axis which leads to increased level of oxygen and nitrous oxide free radicals and proinflammatory leukotrienes (49). 

Flavonoids have also anti-inflammatory activity. It has been found to have in addition to the strong antioxidant activity, an eicosanoid enzyme inhibition property (50). Studies suggested that bioflavonoids may be a potential lead for a new type of anti-inflammatory agents having dual inhibitory activity of group 11 phospholipase A and cyclooxygenase. It has been proved by animal experimental studies that it has both anti-inflammatory and analgesic property (51). 

Flavonoids are natural products widely distributed in the vegetable kingdom and are capable of modulating the activity of enzymes that affect the behavior of many cell systems, suggesting that these compounds may possess significant antiallergic in addition to the anti-inflammatory activities (52). There have been numerous topical applications of plant extracts having flavonoids known as anti-inflammatory compounds. The anti-inflammatory activities, of some plants have been attributed at least in part to the inhibition of arachidonic acid cascade related enzymes by flavonoids (53). The effect of naturally occurring flavonoids on epidermal cyclooxygenas/lipoxygenase was studied. The eicosanoid generated in the epidermis are believed to be involved in various biological activities of the skin. Experimental studies showed that flavonoids inhibit cyclooxygenase and lipoxygenase in various degrees, which explains their anti-inflammatory effect (54). 

Flavonoids have been found to display significant antifungal activity (55). A group of polyphenolic bioflavonoids, Proanthocyanidins, have been reported to exhibit a wide range of biological, pharmacological and chemoprotective properties against oxygen free radicals (56). Flavonoids works better when applied topically as they are poorly absorbed from the gut and are subject to degradation by intestinal microorganisms thus the amount remains biologically available may not be of sufficient concentration (57). 

The clinical effect of bioflavonoids combined with ascorbic acid has been found to have beneficial effect in treating chronic progressive pigmented purpura as it increases capillary resistance and mediates potent antioxidative radical scavenging activities (58). Animal experimental studies showed that flavonoids have protective activity against skin vascular permeability (59). 

The stratum corneum, the outermost barrier of the body is frequently and directly exposed to a pro-oxidative environment, including ultraviolet solar radiation. Depletion of vitamin E, being the major lipophilic antioxidant is an early and sensitive in vivo marker of UV induced photo-oxidation (60). UV radiation causes acute adverse effects like sunburn, photosensitivity reactions, or immunologic suppression, as well as long-term sequelae like photoaging or malignant skin tumors. Combined vitamins C and E reduce the sunburn reaction, which might indicate a consequent reduced risk of later sequelae (61). 

Studies showed that alpha-tocopherol inhibits UVR- induced epidermal lipid peroxidation, suggesting that this may be one mechanism by which alpha-tocopherol prevents UVR-induced local Immunosuppression. Scavenging of UVR- generated lipid peroxides and reactive oxygen may inhibit loss of cell membrane integrity preventing depletion of lymphocyte numbers, thus protecting from local Immunosuppression (62). 

However, application of alpha-tocopherol rich oil before exposure to UVR results in preservation of vitamin E (63). Animal experimental studies showed that topical application of alpha-tocopherol, the most prominent naturally occurring form of vitamin E, inhibits ultraviolet induced photocarcinogenesis and DNA photodamage. The topical application of alpha tocopherol at least 2 hours before exposure to sun is important to allow enough time for cellular uptake of alpha -tocopherol as this is necessary for their optimal photoprotection (64). Clinical studies showed that alpha-tochopherol act synergistically with Ascorbic acid and protect the skin against solar stimulated radiation induced skin inflammation and so suppress the sunburn reaction in healthy volunteers (65). 

The presence of ozone (O (3)) in photochemical smog is considered another important health concern. The stratum corneum (SC), the outermost skin layer and the permeability barrier of the skin, represents a sensitive target for O (3)-induced oxidative stress and depletion of vitamin E. Remarkably, repeated low-level O (3) exposures resulted in cumulative oxidative effects in the stratum corneum (66). It has been found that damage of the cutaneous lipids caused by ozone exposure, is an effect that can be attenuated by vitamin E application (67). 

Studies showed that vitamin E increased the stratum corneum hydration statistically significantly. There was also evidence of an enhanced water-binding capacity after treatment with vitamin E. For the hydrating effect of vitamin E its concentration is of importance. The optimum concentration turned out to be 5% (68). 

Alpha-tocopherol has been found to negatively regulate proliferation of human skin fibroblasts and reduce the signs of aging, as cell proliferation is an important event in the aging process. . When alpha-tocopherol was added to the growth medium at a physiological concentration of 50 microM, cell proliferation was inhibited by 40% in 72 h. Both the duration and concentration of the alpha-tocopherol are important parameters of controlling the proliferation process (69). 

The alpha-tocopherol topical treatment increased alpha- tocopherol levels both in the epidermis (62-fold) and the dermis (22-fold), further more it reduces the formation of epidermal lipid hydroperoxides after UV irradiation. Studies showed that topical alpha-tocopherol application enhance the level of epidermal and dermal antioxidants and prevent ultra violet oxidative damage of cutaneous tissue. The underlying mechanism of this effect involves the up-regulation of a network of enzymatic and non -enzymatic antioxidants (70). After topical application of alpha-tocopherol the stratum corneum was found to contain the highest concentration of vitamin E per micro m. thickness. The largest fraction of skin vitamin E following topical application was found in the deeper subcutaneous layer-the lowest layer, the papillary dermis and the dermis contained the major portion of the of the applied vitamin E. Although the papillary epidermis only represents about 16% of the total skin thickness, it contains sebaceous glands, lipid secretory organs and thus may account for the vitamin E affinity of this layer. Hence applied vitamin E penetrates rapidly through the skin but the highest concentrations are found in the uppermost 5 microns (71). 

Studies showed that glycolic acid could strongly potentiate the antioxidant action of vitamin E. This suggests the advantage of combining alpha-glycolic acid with these antioxidants in skin-designed preparations, both to improve penetration and availability of antioxidants to epidermal layers and to enhance their protective potential (72). 

Vitamin A is the generic term for a variety of fat-soluble substances including retinol, retinylaldhyde and retinoic acid. Vitamin A is commonly known as the anti-infective vitamin and has an essential role in cellular differentiation, the latter providing a unique core mechanism helping to explain the influence of vitamin A on epithelial barriers. Vitamin A has an influence on epithelial barrier. Alterations in the epithelial lining of vital organs occur early in deficiency, suggesting a potentially important role for the barrier function (73). 

Topical retinoic acid (RA) causes irritation of the skin. To prevent this side effect, natural precursors of retinoic acid have been proposed. The natural retinoids (retinol and retinaldehyde have been found to have a good tolerance profile, in contrast with the irritating potential of retinoic acid (74). However, retinol and retinaldhyde are metabolized by the dermis into retinoic acid. After treatment with retinol and retinaldhyde, low but significant amounts of retinoic acid could be detected in the epidermis, as well as in the dermis. In comparison, treatments with retinoic acid itself, leads to higher level of retinoic acid in the epidermis and in the dermis. Thus the low proportion of retinaldehyde, metabolized into a -tran-retenoic acid, explains the low irritancy profile of topical retinaldehyde and supports the concept of controlled delivery of ligands. Thus the action of retinol or retinaldhyde on the skin is still via a retinoic acid formation through the metabolic function of the dermis (75).

Retinaldehyde (RAL), a natural metabolite of beta-carotene and retinol (ROL), can be used topically in human skin and exerts biological activity; it may be a convenient way to deliver multipotential vitamin A activity in epidermis. Animal experiments indicated that keratinocytes metabolise topical retinaldehyde. Keratinocytes differentiating in vitro exhibit greater capacity for retinoic acid synthesis from retinol or retinaldehyde as compared to nondifferentiated cells (76). Experimental study results suggest that increasing cellular concentration of retinoic acids in in-vitro differentiating keratinocytes is achieved by a process of increased activity of the retinoic acid synthesis (77). Thus the concept of using retinaldehyde as a precursor has been confirmed. The keratinocytes predominantly channel retinaldhyde into storage forms should also be considered as a convenient way to load the epidermis with vitamin A. 

It has also been found that after experimental topical application of retinol and retinaldhyde that there was a significant amount of 14-hydroxy-4, 14-retro-ROL (14-HRR), a metabolite that could promote the growth of B lymphocytes (humeral antibodies) and activate T-lymphocytes (cellular immunity), suggests distinct potentials of topical retinol and retinaldhyde (78). 

Studies showed that topical retinol appears to improve the resistance of the stratum corneum against some chemical and physical (UV) threat. It also limits UV-induced shallow wrinkling (79). 

Retinoids was found to inhibit proliferation of melanocytes and melanoma cells and affect disorders of hypo- and hyperpigmentation. The endogenous concentrations of retinol and its metabolites in melanocytes were found to be five times those in melanoma cells. Dissimilarities in the metabolism and endogenous concentration of retinoids between benign and malignant melanocytes might play a key role in differentiation and growth regulation (80). 

Vitamin C (Ascorbic, Ascorbate) is an essential micronutrient involved in many biologic and biochemical functions. Humans cannot synthesize vitamin C because they lack the last enzyme in biosynthetic pathway. Known functions of vitamin C are accounted for by its action as an electron donor or reducing agent. Vitamin C is a specific electron donor for 8 enzymes (81,82). Three of them are enzymes that participate in collagen hydroxylation (important step for keeping a healthy skin. Vitamin C also has non-enzymatic-reductive functions in chemical reactions. Based on its free radical intermediate, vitamin C is a chemical reducing agent (antioxidant) in many intracellular and extracellular reactions. Vitamin c could also decrease oxidative damage in vascular walls (83,84). 

Environmental exposure to ultraviolet light B (UVB, wave lengths 290-320 nm) of the solar spectrum causes major damage, including an inflammatory response, in skin. Studies using the human keratinocyte cell line, showed that stable derivative of ascorbic acid, are able to reduce UVB damage. These data suggest that ascorbic acid shows a photoprotective effect against UVB-induced inflammation and damage in human epithelial cells (85). Topical application of ascorbic acid suppresses the cutaneous inflammation induce by ultraviolet irradiation in human and animals. Studies suggested that it prevents the acute inflammation partly through scavenging reactive oxygen species and potentiating the antioxidative activity of alpha-tocopherol (86). Experimental studies showed that ascorbic acid inhibited UVA-induced lipid peroxidation in cultured human keratinocytes in a concentration-dependent manner. 

It has also been found that ascorbic acid was able to down regulate the proinflammatory cytokines IL-alpha and IL-6. These findings indicate a major cell-protective effect of ascorbic acid on UVA-induced lipid peroxidation and the secretion of pro-inflammatory cytokines by UVA irradiated human keratinocytes (87). 

Calendula Officinalis L has gained importance in the process of rediscovering natural healing forces. Increasing significance is contributed to calendula ointment, which have been used traditionally for a long time

Calendula extracts is characterized by a high level of terpenoids e.g. saponosides in the form of oleanolglycosides and triterpene alcohols. The triterpenediol-3-monoesters consist for 85% of Faradiol esters. 

Calendula extract is a rich source of carotinoids. The colour of the flowers depends on their content of carotinoids (88). 

Also remarkable is the fat oil of the seeds which predominately consists of the conjugated trienoic calendula acid (88). 

Calendula preparations are mainly used for the treatments of wounds and for cosmetical purposes (88). Dressing materials containin Calendula Officinalis ointment applied to experimental animal's wounds has been found to enhance the tissue repair (89). Topical application of Calendula Officinalis markedly stimulates physiological regeneration and epithelization. This effect is assumed to be due to more intensive metabolism of glycoproteins, nucleoproteins and collagen proteins during the regenerative period in the tissue (90). Medicinal herbs containing Calendula extract has been found to be stimulating to the wound healing process by their antifungal/antibacterial qualities. Some investigators reported that the wound-healing period for Calendula Officinalis is shorter than that of the witness (91). 

Animal experimental studies showed that the green leaf juice of C. Officinalis produced significant analgesia; pain threshold increased by 58.9 and 62.15 to that of control. It has been also found to have anti-inflammatory action (92). 

Studies proved the anti-inflammatory action of Calendula Officinalis (93). The triterpenoids has been shown to be the most important anti-inflammatory principles of Calendula extracts. The anti-inflammatory activity was proportional to their content of Faradiol monoester, which can be taken as a suitable parameter for the quality control of Calendula preparations (94, 95). Whole plant extract differ from that of the flowers by the presence of monoterpene hydrocarbons, essential oil, in addition to the alcohols

Calendula Officinalis extracts has been found to have anti-edematous activity due to its Faradiol esters content which is dose dependent activity (96). 

Calendula extract is a rich source of Flavonoids. Characteristic calendula-flavonoids are the isorhamnetin glycosides. The total flavonoids in calendula Officinalis flowers in the ligulate rayflorets and tubular disc-florets were found to be 0.88 and 0.25% respectively (97). 

The saponins isolated from Calendula Officinalis were tested for its toxic and mutagenic activities. All the saponins were found to be non-toxic and non-mutagenic for doses of g (98). 

In a multicentre observational study, 127 patients with various types of dermatitis were administered a homeopathic complex including viola tricolor. In 119 of 127 cases, clear improvement with no side effects was observed (99). 

Viola tricolor extract is a rich source of antioxidants. The total flavonoid contents were determined using rutin as the standard. Rutin content was highest in Viola tricolor flowers among 11 plants species collected in Turkey (100). 

Extract of viola tricolor was found to have antifungal activity and is effective against trichophyton mentagrophytes (101). 

It exhibits antihistaminic effect. Animal experimental studies showed that en-yen dicycloether fraction of the essential oil of chamomile inhibits the release of histamine from the protamine sulphate-provoked degranulation of mast cells, which is the cause of allergic symptoms (102). 

Chamomile extract has been found to exert anti-inflammatory activity in vivo, and so it is used for the treatment of inflammatory skin diseases. Its activity is due to the Chamazulene component of the extract, which inhibits the formation of leukotriene B-4 in neutrophilic granulocytes and additional antioxidative effect lead to blocking the chemical peroxidation of arachidonic acid (103). 

It has also been proved by experimental studies that chamomile extract demonstrated clear antidermatophytic activity (104). 

Animal experimental study showed that a long-term exposure to low doses of the heteropolysaccharides from chamomile flowers enhance the immune response to bacterial infection and it has been concluded that chamomile extract has the ability to modulate the immune system (105). From the essential oil components: alpha-bisabolol and Chamazulene has the strongest activity on Gram-positive and Gram-negative bacteria and on pathogenic fungi (106). 

The fruits of Rosa canina (Rosaceae) are very rich in carotenoids. Chromatographic analysis revealed the major carotenoids to be beta-carotene, lycopene, beta-chryptoxanthin, rubixanthin, zeaxanthin and lutein (107). 

Rosa canina contains vitamin C content is in high proportions. The analysis showed the vitamin C contents were 1200-mg/100 g in the frozen fruits and 2000 mg/100 g in the dried fruits (108). 

Extracts of Rosa canina routs showed anti-inflammatory activity. Laboratory experiments showed its in vitro inhibitory effects on interleukin-1 (IL-1alpha, IL-beta) and tumor necrosis factor (TNF- alpha) biosynthesis in various percentages depending upon the concentration that explains its anti-inflammatory effect and support their folkloric utilization (109). 

The efficacy of the Echinacea root extract as an immunomodulatory has been demonstrated in studies of viral and bacterial infection. The therapeutic superiority of the herbal immunomodulatory over placebo was confirmed as statistically significant and clinically relevant. Studies also demonstrated its efficacy as an immunobalancing agent, which is an antigen-independent mode of phytoimmunomodulation (110). 

The mother tinctures of Echinacea have shown high inhibitory effect against Staphylococcus epidermidis (111). 

Topical application of Echinacea containing ointment has been found to have good antiviral activity against both acyclovir resistant and acyclovir susceptible strains of HSV-1 and HSV-2 anti herpes simplex virus (HSV) (112). Laboratory experiments showed that macrophages cultured in concentrations of Echinacea as low as 0.012 mug/ml produced significantly higher levels of IL-1, TNF-alpha, IL-6 and IL-10 than unstimulated control cells. The high levels of IL-1, TNF-alpha, and IL-10 induced by very low levels of Echinacea are consistent with an immune activated antiviral effect (113). 

Echinacea stimulates wound-healing process by their antifungal/antibacterial qualities. Its locally applied form is well received by the tissues, without irritation, their action being primarily local rather than general as has been noticed from the paraclinic exams (114). 

The Echinacea Purpurea flowers have more anti-inflammatory activity than the routs (115). Polyunsaturated alkamides isolated from Echinacea were shown to possess inhibitory activity in in-vitro cyclooxygenase and 5- lipoxygenase (116). 

Echinacea Purpurea stimulates the neutrophil phagocytosis. Echinacea treatment of mice, immunosuppressed with immunosuppressive drugs, restored their resistance against lethal infections with the predominantly granulocyte-dependent Candida albicans through stimulating the phagocytic activity (117,118). Polysaccharides purified from Echinacea purpurea were found to have antistaphylococci activity. These substances enhanced the ability of granulocytes to kill staphylococci. Also activate monocytes to secrete TNF-alpha, IL-6 and IL-1. Altogether, as in mice, the polysaccharides could induce acute phase reactions and activation of phagocytes in human (119). 


(1) Henry F. Rakic L. Van Cromphaut I. Pierard-Franchimont C. Pierard GE. [Skin microcirculation, adherence molecules and inflammatory dermatoses]. [Review] [15 refs] [French] Revue Medicale de Liege. 53(8):479-82, 1998 Aug.
(2) Robert, Caroline; Kupper, Thomas S.Mechanisms of Disease: Inflammatory Skin Diseases, T Cells, and Immune Surveillance Volume 341(24) 9 December 1999 pp 1817-1828.

(3) Hanifin JM. Atopic dermatitis. In: Middleton E, Reed CE, Ellis EF, Adkinson NF, Yunginger JW, Busse WW, eds. Allergy principles and practice, 4th edn. St Louis: Mosby, 1993: 1581-604. Rudikoff, Donald; Lebwohl, Mark Atopic dermatitis [Seminar] Lancet 1998; 351: 1715-21.

(4) Dahl RE, Bernhisel-Broadbent J, Scanlon-Holdford S, Sampson HA, Lupo M. Sleep disturbances in childen with atopic dermatitis. Arch Pediatr Adolesc Med 1995; 149: 856-60. 

(5) Picker LJ, Treer JR, Ferguson-Darnell B, Collins PA, Bergstresser PR, Terstappen LW. Control of lymphocyte recirculation in man. II. Differential regulation of the cutaneous lymphocyte-associated antigen, a tissue-selective homing receptor for skin-homing T cells. J Immunol 1993;150:1122-36.

(6) Imokawa G, Abe A, Jin K, Higaki Y, Kawashima M, Hidano A. Decreased level of ceramides in stratum corneum of atopic dermatitis: an etiologic factor in atopic dry skin? J Invest Dermatol 1991; 96: 523-26. 

(7) Murata Y, Ogata J, Higaki Y, et al. Abnormal expression of sphingomyelin acylase in atopic dermatitis: an etiologic factor for ceramide deficiency? J Invest Dermatol 1996; 106: 1242-49. 

(8) Seguchi T, Chang-Yi C, Kusuda S, Takahashi M, Aisu K, Tezuka T. Decreased expression of filaggrin in atopic skin. Arch Dermatol Res 1996; 288: 442-46. 

(9) Hanifin JM, Rakja G. Diagnostic features of atopic dermatitis. Acta Dermatovener 1980; 92 (suppl): 44-47.

(10) Aly R, Mailbach HI, Shinefield HR. Microbial flora of atopic dermatitis. Arch Dermatol 1977; 113: 780-82.

(11) Dahl RE, Bernhisel-Broadbent J, Scanlon-Holdford S, Sampson HA, Lupo M. Sleep disturbances in childen with atopic dermatitis. Arch Pediatr Adolesc Med 1995; 149: 856-60.

(12) Robert, Caroline; Kupper, Thomas S.Mechanisms of Disease: Inflammatory Skin Diseases, T Cells, and Immune Surveillance Volume 341(24) 9 December 1999 pp 1817-1828 

(13) Butcher EC, Picker LJ. Lymphocyte homing and homeostasis. Science 1996;272:60-6.
(14) Picker LJ, Treer JR, Ferguson-Darnell B, Collins PA, Bergstresser PR, Terstappen LW. Control of lymphocyte recirculation in man. II. Differential regulation of the cutaneous lymphocyte-associated antigen, a tissue-selective homing receptor for skin-homing T cells. J Immunol 1993; 150:1122-36.

(15) Picker LJ, Treer JR, Ferguson-Darnell B, Collins PA, Bergstresser PR, Terstappen LW. Control of lymphocyte recirculation in man. II. Differential regulation of the cutaneous lymphocyte-associated antigen, a tissue-selective homing receptor for skin-homing T cells. J Immunol 1993; 150:1122-36 

(16) Picker LJ, Treer JR, Ferguson-Darnell B, Collins PA, Bergstresser PR, Terstappen LW. Control of lymphocyte recirculation in man. II. Differential regulation of the cutaneous lymphocyte-associated antigen, a tissue-selective homing receptor for skin-homing T cells. J Immunol 1993; 150:1122-36.

(17) Leung, S.Y.M.; Hauk, P.; Strickland, l.;Travers, J.B.; Norris, D.A. The role of superantigens in human diseases: therapeutic implications for the treatment of skin diseases ] British Journal of Dermatology, Supplement. 139 (Supplement 53):17-29,
December 1998.
(18) Bruch-Gerharz, Daniela; Ruzicka, Thomas; Kolb-Bachofen, Victoria * Nitric Oxide in Human Skin: Current Status and Future Prospects. Journal of Investigative Dermatology. 110(1): 1-7, January 1998.

(19) de Groot AC. van Ginkel CJ. Bruynzeel DP. [Contact allergy for corticosteroids]. [Review] [22 refs] [Dutch] Nederlands Tijdschrift voor Geneeskunde. 141(32): 1559-62, 1997 Aug 9.

(20) Krutmann J. Phototherapy for atopic dermatitis. Dermatol Ther 1996; 1: 24-31.

(21) Berth-Jones J, Graham-Brown RA, Marks R, et al. Long term efficacy and safety of cyclosporin in severe adult atopic dermatitis. Br J Dermatol 1997; 136: 76-81. 

(22) Lear JT, English JSC, Jones P, Smith AG. Retrospective review of the use of azathioprine in severe atopic dermatitis. J Am Acad Dermatol 1996; 35: 642-43. 

(23) Tan BB. Azathioprine in dermatology: a survey of current practice in the UK. Br J Dermatol 1997; 136: 351-55. 

(24) Mennet-Von Eiff M. Meier B. Phytotherapy in dermatology. 9th Swiss Congress for Phytotherapy. Zeitschrift fur Phytotherapie. Vol 16(4) (pp 201-210), 1995.
(25) Bresser H. Flach D. Hartung A. Krautheimer B. Zenker C. New aspects in the treatment of neurodermatitis and dermatitis. Arztez Naturheil Verfahren. Vol 40(8) (pp 558-562), 1999.
(26) Lichnerov I. Masterova I. Formulation of creams containing extracts from calendula officinalis L. Ceska a Slovenska Farmacie. Vol 47(2) (pp 79-83), 1998.

(27) Carson C F. Riley T V. American Journal of Infection Control 24(3). 1996. 186-189).

(28) Raman A. Weir U. Bloomfield S F. Letters in Applied Microbiology 21(4). 1995. 242-245).
(29) Carson C F. Riley T V. Letters in Applied Microbiology 19 (1). 1994. 24-25.
(30) Carson C F. Cookson B D. Farrelly H D. Riley T V. Journal of Antimicrobial Chemotherapy 35(3). 1995. 421-424)
(31) Nenoff P [a]. Haustein U-F. Brandt W.Antifungal activity of the essential oil of Melaleuca alternifolia (Tea Tree Oil) against pathogenic fungi in vitro. Skin Pharmacology. 9(6). 1996. 388-394. 
(32) Bassett I B. Pannowitz D L. Barnetson R S C. Medical Journal of Australia 153 (8). 1990. 455-456, 458.

(33) Ziboh VA. The significance of polyunsaturated fatty acids in cutaneous biology. Lipids. 31 Suppl: S249-53, 1996 Mar.
(34) Punnonen K. Puustinen T. Jansen CT. Time course of incorporation of 20-carbon polyunsaturated fatty acids in a human keratinocyte cell line. Lipids. 22(3): 139-43, 1987 Mar.
(35) Nicollier M. Massengo T. Remy-Martin JP. Laurent R. Adessi GL. Free fatty acids and fatty acids of triacylglycerols in normal and hyperkeratotic human stratum corneum. Journal of Investigative Dermatology. 87(1): 68-71, 1986 Jul. 

(36) Henz B M [a]. Jablonska S. Van De Kerkhof P C M. Stingl G. Blaszczyk M. Vandervalk P G M. Veenhuizen R. Muggli R. Raederstorff D.Double-blind, multicentre analysis of the efficacy of borage oil in patients with atopic eczema. British Journal of Dermatology. 140(4). April, 1999. 685-688. 

(37) Wertz PW. Downing DT. Metabolism of topically applied fatty acid methyl esters in BALB/C mouse epidermis. Journal of Dermatological Science. 1(1):33-7, 1990 Jan.
(38) Huang Fang-Cheng. Ju Yi-Hsu [a]. Chiang Jen-Chung. gamma-Linolenic acid-rich triacylglycerols derived from borage oil via lipase-catalyzed reactions. Journal of the American Oil Chemists Society. 76(7). July 1999. 833-837. 
(39) San Juan P M F. Study of the presence of Gamma Linolenic Acid in vegetable oils. Alimentaria 29 (231). 1992. 49-52.

(40) Tollesson Anders [a]. Frithz Anders. Transepidermal water loss and water content in the stratum corneum in infantile seborrhoeic dermatitis. Acta Dermato-Venereologica. 73(1). 1993. 18-20.

(41) Ziboh V A. Fletcher M P. Dose-response effects of dietary Gamma Linolenic Acid-eriched oils on human polymorphonuclear-neutrophil biosynthesis of leukotriene B-4 American Journal of Clinical Nutrition 55 (1). 1992. 39-45.
(42) Miller C C. Tang W. Ziboh V A. Fletcher M P. Dietary supplementation with ethyl ester concetrates of fish oil N-3 and borage oil N-6 polyunsaturated fatty acids induces epidermal generation of local putative anti-inflammatory metabolites. Journal of Investigative Dermatology 96 (1). 1991. 98-103. 

(43) Belury MA. Leyton J. Patrick KE. Cumberland AG. Locniskar M. Fischer SM. Modulation of phorbol ester-elicited events in mouse epidermis by dietary n-3 and n-6 fatty acids. Prostaglandins Leukotrienes & Essential Fatty Acids. 44(1):19-26, 1991 Sep.

(44) Gron B. Iversen L. Ziboh V. Kragballe K. Distribution of monohydroxy fatty acids in specific human epidermal phospholipids. Dermatology. 2(1): 38-44, 1993 Feb.

(45) Hassig A [a]. Liang W X. Schwabl H. Stampfli K. Flavonoids and tannins: Plant-based antioxidants with vitamin character. Medical Hypotheses. 52(5). May, 1999. 479-481.

(46) Mauri Pier Luigi [a]. Iemoli Loredana. Gardana Claudio. Riso Patrizia. Simonetti Paolo. Porrini Marisa. Pietta Pier Giorgio. Liquid chromatography/electrospray ionization mass spectrometric characterization of flavonol glycosides in tomato extracts and human plasma. Rapid Communications in Mass Spectrometry. 13(10). 1999. 924-931. 

(47) Duthie S J [a]. Dobson V L. Dietary flavonoids protect human colonocyte DNA from oxidative attack in vitro. European Journal of Nutrition. 38(1). Feb., 1999. 28-34. 

(48) Jeong Hyeh-Jean. Shin Young Geun. Kim Il-Hyuk. Pezzuto John M [a]. Inhibition of aromatase activity by flavonoids. Archives of Pharmacal Research (Seoul). 22(3). June, 1999. 309-312 . 

(49) Paladini A C [a]. Marder M [a]. Viola H. Wolfman C. Wasowski C. Medina J H. Flavonoids and the central nervous system: From forgotten factors to potent anxiolytic compounds. Journal of Pharmacy & Pharmacology. 51(5). May, 1999. 519-526. 

(50) Schubert Shay Yehoshua. Lansky Ephraim Philip. Neeman Ishak [a]. Antioxidant and eicosanoid enzyme inhibition properties of pomegranate seed oil and fermented juice flavonoids. Journal of Ethnopharmacology. 66(1). July, 1999. 11-17.

(51) Kim Hee Kee. Son Kun Ho. Chang Hyeun Wook. Kang Sam Sik. Kim Hyun Pyo [a]. Amentoflavone, a plant biflavone: A new potential anti-inflammatory agent. Archives of Pharmacal Research (Seoul). 21(4). Aug., 1998. 406-410. 

(52) Di Carlo Giulia. Mascolo Nicola. Izzo Angelo A. Capasso Francesco [a]. Flavonoids: Old and new aspects of a class of natural therapeutic drugs. Life Sciences. 65(4). June 18, 1999. 337-353.

(53) Moon Tae Chul [a]. Park Jeong Ok [a]. Chung Kwang Won [a]. Son Keun Ho. Kim Hyun Pyo. Kang Sam Sik. Chang Hyeun Wook [a]. Chung Kyu Charn [a]. Anti-inflammatory activity of the flavonoid components of Lonicera japonica. [Korean] Yakhak Hoeji. 43(1). Feb., 1999. 117-123. 

(54) Kim HP. Mani I. Iversen L. Ziboh VA. Effects of naturally-occurring flavonoids and biflavonoids on epidermal cyclooxygenase and lipoxygenase from guinea-pigs. Prostaglandins Leukotrienes & Essential Fatty Acids. 58(1):17-24, 1998 Jan.

(55) Lopes Norberto P. Kato Massuo J [a]. Yoshida Massayoshi. Antifungal constituents from roots of Virola surinamensis. Phytochemistry (Oxford). 51(1). May, 1999. 29-33. 

(56) Bagchi D. Garg A. Krohn R L. Bagchi M. Tran M X. Stohs S J [a]. Oxygen free radical scavenging abilities of vitamins C and E, and a grape seed proanthocyanidin extract in vitro. Research Communications in Molecular Pathology & Pharmacology. 95(2). 1997.179-189. 

57) Formica J V [a]. Regelson W. Review of the biology of quercetin and related bioflavonoids. Food & Chemical Toxicology. 33(12). 1995. 1061-1080. 

(58) Reinhold U. Seiter S. Ugurel S. Tilgen W. Treatment of progressive pigmented purpura with oral bioflavonoids and ascorbic acid: an open pilot study in 3 patients. Journal of the American Academy of Dermatology. 41(2 Pt 1):207-8, 1999 Aug.

(59) Budzianowski J. Korzeniowska K. Chmara E. Mrozikiewicz A. Microvascular protective activity of flavonoid glucuronides fraction from Tulipa gesneriana. Phytotherapy Research. 13(2):166-8, 1999 Mar.

(60) Thiele JJ. Traber MG. Packer L. Depletion of human stratum corneum vitamin E: an early and sensitive in vivo marker of UV induced photo-oxidation. Journal of Investigative Dermatology. 110(5):756-61, 1998 May.

(61) Eberlein-Konig B. Placzek M. Przybilla B. Protective effect against sunburn of combined systemic ascorbic acid (vitamin C) and d-alpha-tocopherol (vitamin E). Journal of the American Academy of Dermatology. 38(1):45-8, 1998 Jan.

(62) Yuen KS. Halliday GM. alpha-Tocopherol, an inhibitor of epidermal lipid peroxidation, prevents ultraviolet radiation from suppressing the skin immune system. Photochemistry & Photobiology. 65(3):587-92, 1997 Mar.

(63) Weber C. Podda M. Rallis M. Thiele JJ. Traber MG. Packer L. Efficacy of topically applied tocopherols and tocotrienols in protection of murine skin from oxidative damage induced by UV-irradiation. Free Radical Biology & Medicine. 22(5):761-9, 1997.

(64) McVean M. Liebler DC. Prevention of DNA photodamage by vitamin E compounds and sunscreens: roles of ultraviolet absorbance and cellular uptake. Molecular Carcinogenesis. 24(3):169-76, 1999 Ma

(65) Fuchs J. Kern H. Modulation of UV-light-induced skin inflammation by D-alpha-tocopherol and L-ascorbic acid: a clinical study using solar simulated radiation. Free Radical Biology & Medicine. 25(9):1006-12, 1998 Dec.

(66) Thiele JJ. Traber MG. Polefka TG. Cross CE. Packer L. Ozone-exposure depletes vitamin E and induces lipid peroxidation in murine stratum corneum. Journal of Investigative Dermatology. 108(5):753-7, 1997 May.

(67) Thiele JJ. Traber MG. Podda M. Tsang K. Cross CE. Packer L. Ozone depletes tocopherols and tocotrienols topically applied to murine skin. FEBS Letters. 401(2-3):167-70, 1997 Jan 20.

(68) Gehring W. Fluhr J. Gloor M. Influence of vitamin E acetate on stratum corneum hydration. Arzneimittel-Forschung. 48(7):772-5, 1998 Jul. 

(69) Onat D. Boscoboinik D. Azzi A. Basaga H. Effect of alpha-tocopherol and silibin dihemisuccinate on the proliferation of human skin fibroblasts. Biotechnology & Applied Biochemistry. 29 ( Pt 3):213-5, 1999 Jun.

(70) Lopez-Torres M. Thiele JJ. Shindo Y. Han D. Packer L. Topical application of alpha-tocopherol modulates the antioxidant network and diminishes ultraviolet-induced oxidative damage in murine skin.British Journal of Dermatology. 138(2):207-15, 1998 Feb.

(71) Traber MG. Rallis M. Podda M. Weber C. Maibach HI. Packer L. Penetration and distribution of alpha-tocopherol, alpha- or gamma-tocotrienols applied individually onto murine skin. Lipids. 33(1):87-91, 1998 Jan.

(72) Morreale M. Livrea MA. Synergistic effect of glycolic acid on the antioxidant activity of alpha-tocopherol and melatonin in lipid bilayers and in human skin homogenates. Biochemistry & Molecular Biology International. 42(6):1093-102, 1997 Sep.

(73) McCullough FS. Northrop-Clewes CA. Thurnham DI. The effect of vitamin A on epithelial integrity. [Review] [37 refs] Proceedings of the Nutrition Society. 58(2):289-93, 1999 May.

(74) Fluhr JW. Vienne MP. Lauze C. Dupuy P. Gehring W. Gloor M. Tolerance profile of retinol, retinaldehyde and retinoic acid under maximized and long-term clinical conditions. Dermatology. 199 Suppl 1:57-60, 1999.

(75) Bailly J. Crettaz M. Schifflers MH. Marty JP. In vitro metabolism by human skin and fibroblasts of retinol, retinal and retinoic acid. Experimental Dermatology. 7(1):27-34, 1998 Feb. 

(76) Siegenthaler et al. 1990. Biochem. J. 268: 371-378. 

(77) Chatellard-Gruaz D. Randolph RK. Hagens G. Saurat JH. Siegenthaler G. Differentiation of human epidermal keratinocytes is accompanied by increased expression of CRABP-II and increased cellular concentration of retinoic acids: retention of newly synthesized retinoic acids by CRABP-II. Journal of Lipid Research. 39(7):1421-9, 1998 Jul. 

(78) Sass JO. Didierjean L. Carraux P. Plum C. Nau H. Saurat JH. Metabolism of topical retinaldehyde and retinol by mouse skin in vivo: predominant formation of retinyl esters and identification of 14-hydroxy-4, 14-retro-retinol. Experimental Dermatology. 5(5):267-71, 1996 Oct.

(79) Goffin V. Henry F. Pierard-Franchimont C. Pierard GE. Topical retinol and the stratum corneum response to an environmental threat. Skin Pharmacology. 10(2):85-9, 1997.

(80) Rosdahl I. Andersson E. Kagedal B. Torma H. Vitamin A metabolism and mRNA expression of retinoid-binding protein and receptor genes in human epidermal melanocytes and melanoma cells. Melanoma Research. 7(4):267-74, 1997 Aug.

(81) Levine M. New concepts in the biology and biochemistry of ascorbic acid. N Engl J Med. 1986;314:892-902. 

(82) Levine M, Rumsey SC, Wang Y, et al. Vitamin C. In: Filer LJ, Ziegler EE, eds. Present Knowledge in Nutrition. Washington, DC: International Life Sciences Institute; 1996:146-159. 

(83) Diaz MN, Frei B, Vita JA, et al. Antioxidants and atherosclerotic heart disease. N Engl J Med. 1997;337:408-416. 

(84) Levine M. Rumsey SC. Daruwala R. Park JB. Wang Y. Criteria and recommendations for vitamin C intake. JAMA. 281(15):1415-23, 1999 Apr 21.

(85) Miyai E. Yanagida M. Akiyama J. Yamamoto I. Ascorbic acid 2-O-alpha-glucoside, a stable form of ascorbic acid, rescues human keratinocyte cell line, SCC, from cytotoxicity of ultraviolet light B. Biological & Pharmaceutical Bulletin. 19(7):984-7, 1996 Jul.

(86) Miyai E. Yanagida M. Akiyama J. Yamamoto I. Ascorbic acid 2-O-alpha-glucoside-induced redox modulation in human keratinocyte cell line, SCC: mechanisms of photoprotective effect against ultraviolet light B. Biological & Pharmaceutical Bulletin. 20(6):632-6, 1997 Jun.

(87) Tebbe B. Wu S. Geilen CC. Eberle J. Kodelja V. Orfanos CE. L-ascorbic acid inhibits UVA-induced lipid peroxidation and secretion of IL-1alpha and IL-6 in cultured human keratinocytes in vitro. Journal of Investigative Dermatology. 108(3): 302-6, 1997 Mar.

(88) Isaac O. Calendula officinalis L. - Marigold. Zeitschrift fur Phytotherapie. Vol 15(6) (pp 356-370), 1994. 

(89) Ansari M A. Jadon N S. Singh S P. Kumar Amresh. Singh Harpal. Effect of Calendula officinalis ointment, charmil and gelatin granules on wound healing in buffaloes: A histological study. Indian Veterinary Journal. 74(7). 1997. 594-597. 

(90) Klouchek-Popova E. Popov A. Pavlova N. Krusteva S. Influence of the physiological regeneration and epithelialization using fractions isolated from Calendula officinalis. Acta Physiologica et Pharmacologica Bulgarica. 8(4):63-7, 1982. 

(91) Oana L. Mates N. Ognean I. Muste A. Aldea Maria. Neculoiu Doris. Banciu Cristina. Studies concerning the wound healing action of some medicinal herb extracts.[Romanian] Buletinul Universitatii de Stiinte Agricole Cluj-Napoca Seria Zootehnie Si Medicina Veterinara. 49(0). 1995. 461-465. 

(92) Hore S K [a]. Koley K M [a]. Maiti S K. [a] Dep. Pharmacology Toxicology, Coll. Veterinary Science A.H., Anjora, Durg 491001 India. Modulatory role of Calendula officinalis on thermal stimulus-induced nociception and carrageenin-induced inflammation in rats. Indian Veterinary Journal. 74(10). Oct., 1997. 844-846. 

(93) Kalvatchev Z. Walder R [a]. Garzaro D.Akihisa Toshihiro [a]. Yasukawa Ken. Oinuma Hirotoshi [a]. Kasahara Yoshimasa. Yamanouchi Sakae. Takido Michio. Kumaki Kunio. Tamura Toshitake [a]. Triterpene alcohols from the flowers of compositae and their anti-inflammatory effects. Phytochemistry (Oxford). 43(6). 1996. 1255-1260. 

(94) Della Loggia R [a]. Tubaro A. Sosa S. Becker H. Saar S. Isaac O. The role of triterpenoids in the topical anti-inflammatory activity of Calendula officinalis flowers. Planta Medica. 60(6). 1994. 516-520. 
(95) Chalchat J C. Garry R P. Michet A. Chemical Composition of Essential oil of Calendula-Officinalis L. Potmarigold Flavour & Fragrance Journal 6 (3). 1991. 189-192. 

(96) Zitterl-Eglseer K [a]. Sosa S. Jurenitsch J. Schubert-Zsilavecz M. Della Loggia R. Tubaro A. Bertoldi M. Franz C. Anti-oedematous activities of the main triterpenediol esters of marigold (Calendula officinalis L.). Journal of Ethnopharmacology. 57(2). 1997. 139-144. 

(97) Masterova I. Grancaiova Z. Uhrinova S. Suchy V. Ubik K. Nagy M. Flavonoids in Flowers of Calendula-Officinalis L Chemical Papers 45 (1). 1991. 105-108.
(98) Elias R. De Meo M. Vidal Ollivier E. Laget M. Balansard G. Dumenil G. Antimutagenic Activity of Some Saponins Isolated From Calendula-Officinalis L. Calendula-Arvensis L. and Hedera-Helix L. Mutagenesis 5 (4). 1990. 327-332.1.

(99) Bresser H. Flach D. Hartung A. Krautheimer B. Zenker C. New aspects in the treatment of neurodermatitis and dermatitis. ARZTEZ NATURHEILVERFAHREN, Vol 40(8) (pp 558-562), 1999.
(100) Toker, G. Turkoz, S. Erdemoglu, N. High performance liquid chromatographic analysis of rutin in plants, I. Pharmazie. 1998. 53: 7, 494-495. 11 ref. 

(101) Guerin, J.-C. Reveillere, H.-P. Antifungal activity of plant extracts used in therapy. I. Study of 41 plant extracts against 9 fungal species. [French] Annales Pharmaceutiques Francaises. 1984. 42: 6, 553-559. 12 ref. 
(102) Miller Thomas. Wittstock Ute. Lindequist Ulrike. Teuscher Eberhard [a]. Effects of some components of the essential oil of chamomile, Chamomilla recutita, on histamine release from rat mast cells. Planta Medica. 62(1). 1996. 60-61. 

(103) Safayhi H [a]. Sabieraj J. Sailer E-R. Ammon H P T. Chamazulene: An antioxidant-type inhibitor of leukotriene B-4 formation. Planta Medica. 60(5). 1994. 410-413. 

(104) Mares D. Romagnoli C. Bruni A. Antidermatophytic activity of herniarin in preparations of Chamomilla recutita (L.) Rauschert. Plantes Medicinales et Phytotherapie. 26(2). 1993. 91-100. 

(105) Laskova I L. Uteshev B S. Immunomodulating action of heteropolysaccharides isolated from chamomile flower clusters. [Russian] Antibiotiki i Khimioterapiya. 37(6). 1992. 15-18. 

(106) Kedzia B. Antimicroorganisms Activity of Ol. Chamomillae and Its Components Herba Polonica 37 (1). 1991. 29-38.

(107) Hodisan Teodor. Socaciu Carmen [a]. Ropan Ioana. Neamtu Gavril. Carotenoid composition of Rosa canina fruits determined by thin-layer chromatography and high-performance liquid chromatography. Journal of Pharmaceutical & Biomedical Analysis. 16(3). Nov., 1997. 521-528. 

(108) Yavru Ilknur. Kadioglu Asim. The effects of infusion temperatures and times on vitamin C content infused from fruits of dog rose (Rosa canina L.). Turkish Journal of Botany. 21(6). 1997. 323-327. 

(109) Yesilada Erdem [a]. Ustun Osman. Sezik Ekrem. Takaishi Yoshihisa. Ono Yukihisa. Honda Gisho. Inhibitory effects of Turkish folk remedies on inflammatory cytokines: Interleukin-1-alpha, interleukin-1-beta and tumor necrosis factor alpha. Journal of Ethnopharmacology. 58(1). 1997. 59-73. 

(110) Wuestenberg P. Henneicke-von Zepelin H-H. Koehler G [a]. Stammwitz U. Efficacy and mode of action of an immunomodulator herbal preparation containing Echinacea, wild indigo, and white cedar. Advances in Therapy. 16(1). Jan.-Feb., 1999. 51-70. 

(111) Bhatt Manoj. Chopra A K. In vitro antimicrobial efficacy of some homoeopathic drugs against Staphylococcus epidermidis. Biological Memoirs. 24(2). Dec., 1998. 31-33. 

(112) Thompson Kenneth D [a]. Antiviral activity of Viraceae against acyclovir susceptible and acyclovir resistant strains of herpes simplex virus. Antiviral Research. 39(1). July, 1998. 55-61. 

(113) Burger Roger A [a]. Torres Anthony R. Warren Reed P. Caldwell Virgil D. Hughes Bronwyn G. Echinacea-induced cytokine production by human macrophages. International Journal of Immunopharmacology. 19(7). July, 1997. 371-379. 

(114) Oana L. Mates N. Ognean I. Muste A. Aldea Maria. Neculoiu Doris. Banciu Cristina. Studies concerning the wound healing action of some medicinal herb extracts. [Romanian] Buletinul Universitatii de Stiinte Agricole Cluj-Napoca Seria Zootehnie Si Medicina Veterinara. 49(0). 1995. 461-465. 

(115) Voitenko H M. Varchenko V H. Lipkan H M. Oliinychenko P I. M'Yasoyedov D V. Mkhitaryan L S. Kutnyak V P. Obedkova N M. Kukhar I V. Yakovlyeva N Yu. Naumova M I. Effect of preparations from roots and flowers of Echinacea purpurea on the progress of inflammatory reaction in experimental conditions. [Ukrainian] Farmatsevtychnyi Zhurnal (Kiev). 0(2). 1996. 115-121. 

(116) Mueller-Jakic Barbara. Breu Walter. Proebstle Andrea. Redl Karl. Greger Harald. Bauer Rudolf [a]. In vitro inhibition of cyclooxygenase and 5-lipoxygenase by alkamides from Echinacea and Achillea species. Planta Medica. 60(1). 1994. 37-40. 

(117) Steinmuelelr Christiane [a]. Roesler Joachim. Groettrup Esther. Franke Gabriela. Wagner Hildebert. Lohmann-Matthes Marie-Louise. Polysaccharides isolates from plant cell cultures of Echinacea purpurea enhance the resistance of immunosuppressed mice against systemic infections with Candida albicans and Listeria monocytogenes. International Journal of Immunopharmacology. 15(5). 1993. 605-614. 

(118) Wagner H. Jurcic K. Immunological Studies of Plant Extract Combinations in-Vitro and in-Vivo on Stimulation of Phagocytosis. Arzneimittel-Forschung 41 (10). 1991. 1072-1076.

(119) Roesler J. Emmendoerffer A. Steinmueller C. Luettig B. Wagner H. Lohmann Matthes M L. Application of Purified Polysaccharides from Cell Cultures of The Plant Echinacea-Purpurea to Test Subjects Mediates Activation of the Phagocyte System . International Journal of Immunopharmacology 13 (7). 1991. 931-942. 

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