There are many herbal formulations are used for treatment psoriasis , But in this paper we will discuss drugs with scientific evidence from publications , books and scientific sites .
New drug developed by Egyptian Dr/agharied consists of aloe vera gel, propolis ( Aloreed ).
Aloe is one of the known herbs in treatment psoriasis . Aloe vera gel is the mucilaginous gel produced from the centre (the parenchyma) of the plant leaf. The gel portion of the plant is prepared by peeling the outer portion of the skin and the pericarp away. It is the preparation which is called ‘pure Aloe vera gel’ in commerce. the condensed juice of Aloe barbadensis leaves. The gel contains enzymes, minerals, vitamins, and saponins and has anti-inflammatory and antibacterial effects. It is commonly added to cosmetics for its moisturizing, regenerative, elasticity-promoting properties, analgesic, antiallergic, antipruritic, wound healing and anti-inflammatory components such as amino acids .
propolis (bee glue) is a sticky dark-colored material that honeybees collect from living plants, mix it with wax and use it in the construction an adaptation of their nests, mainly to fill out cracks in the bee hive. It has been used in folk medicine since ancient times and is now known to be a natural medicine and it varies in some of its components according to source . Whereas bud exudates of different poplar species and clones are frequently similar in qualitative composition, they may differ in their quantitative composition. These differences are reflected in the composition of propolis into which the bud exudate is incorporated .
Raw propolis is composed of approximately 50% resin (polyphenolic fraction), 30% wax, 10% essential oils, 5% pollen and 5% various organic and inorganic compounds Chemical composition of propolis is very complex. More than 200 compounds have been identified . Its biological activity depends on compounds from the polyphenolic fraction, mainly flavonoids, followed by aromatic acids, phenolic acid esters, triterpenes, lignans, etc. It is included in dermatological preparations used for tissue regeneration and wound healing, for the treatment of psoriasis, morphea, herpes simplex and herpes genitalis and anal pruritus, and it is also a component of antidermatophyte preparations, also it has antibacterial, antifungal, antitumoral, antioxidative, imunomodulatory and other beneficial activities .
Theraflax (Department of Dermatology and Venereology, Medical Faculty-sofia,Bulgaria) , which consists of alpha-linolenic acid, linoleic acid, oleic acid, gamma-linolenic acid, palmitic acid and other fatty acids .
Evening primrose (Oenothera biennis) Gamolenic acid and its metabolite dihomogamma-linolenic acid (DGLA) are precursors of both the inflammatory prostaglandin E2 (PGE2) series via arachidonic acid (AA), and of the less inflammatory prostaglandin E1 (PGE1) series. Actions attributed to PGE1 include anti-inflammatory, immunoregulatory and vasodilatory properties, inhibition of platelet aggregation and cholesterol biosynthesis, hypotension and elevation of cyclic AMP (inhibits phospholipase A2 ).
Dietary supplementation with gamolenic acid has been noted to have a favourable effect on the DGLA:AA ratio. Although an increase in arachidonic acid concentrations is also seen, this is much smaller and less consistent compared with the increase seen for DGLA.Contributory factors to this negative effect on arachidonic acid are PGE1 and 15-hydroxy-DGLA. The latter inhibits conversion of arachidonic acid to inflammatory lipoxygenase metabolites including leukotrienes, whilst PGE1 inhibits the enzyme phospholipase A2 which is required for the mobilisation of arachidonic acid from phospholipid membrane stores . Pregnant women should not use evening primrose oil.
Also these drugs as well as linseed (Linum usitatissimum) oil or flax seed oil can modify the metabolic changes associated with psoriasis , as a result of increased percent of saturated fatty acids in blood samples in comparison to the levels of poly un saturated fatty acids (EFA)-linoleic and arachidonic, wich play an important role as structral compounds of membrane cell phospholipids.
Liqourice (Glycyrrhiza glabra) , fenugreek (Trigonella foenum-graecum) and sarsaparilla contain saponins that has anti-inflammatory effect and cortisone like effect as well as flavenoids that found in fenugreek and liqourice .
Ammi majus and angelica (Dong Quay ) contain psoralen ( furano coumarin ) it’s a planner compound can interact with DNA molecules: it was reported that interstrand cross links are formed in native DNA by irradiation with 360 nm light in the presence of psoralen ,and suggested that the cross-link may result from the reaction of an excited psoralen molecule with pyrimidine bases in opposite strands of the DNA duplex. 5-lipoxygenase (5-LO) inhibition with angelica that produce leukotriene B4 which contribute with inflammatory reactions .
Chamomile (Matricaria recutita). The chamomile flowers have a long therapeutic tradition in treating gastrointestinal ailments. The rationale for its use in psoriasis is three-fold. First, chamazulene, a by-product of the non-volatile oil extract, matricin, has anti-inflammatory activity through the inhibition of lipoxygenase and, as a result, leukotriene B4 (LTB4) formation. There is evidence supporting the role of increased LTB4 formation in psoriatic plaques; therefore, inhibition results in disease improvement (Aggag & Yousef, 1972). Second, chamomile oil has antimicrobial activity against skin pathogens, Staphylococcus and Candida (Leung, Walsh, Giorno, & Norris, 1993). Lastly, the flavonoids, quercetin and apigenin, are also active compounds of the flower. Quercetin, a potent inhibitor of lipoxygenase, and to a lesser degree, cyclooxygenase, is readily absorbed through the skin (Brown & Dattner, 1998; Kim, Mani, Iversen, & Ziboh, 1998). As of yet, there are no clinical trials assessing the efficacy and adverse side effect profiles of chamomile reported in the treatment of psoriasis. Contact dermatitis (delayed type hypersensitivity) and systematized allergic response, however, have been reported (Gruenwald, 2004; Paulsen, 2002).
Wintergreen/Boxberry (Gaultheria pro cumbens). Wintergreen is a plant native to the Eastern United States, and historically was used by Native Americans as an analgesic. The methyl salicylate constituent is responsible for its anti-inflammatory properties. Although used topically for psoriasis, wintergreen can cause systemic effects. Brubacher and Hoffman (1996) reviewed 20 cases of systemic salicylate toxicity (tinnitus, vomiting, tachypnea, and acid-base disturbances) from using topical creams (Bell & Duggin, 2002). Pa tients at greatest risk are those using aspirin or a prescribed salicylic acid compound in conjunction with a salicylate herbal (for example, wintergreen, aloe vera, or red clover). Additionally, oil of wintergreen can increase prothrombin time and international normalized ratio of clotting, creating problems for pa tients on warfarin (Chan, 1996). There are no investigations on its effectiveness in psoriasis .
Milk thistle (Silybum marianum). The medicinal utility of milk thistle flower seeds dates back to Pliny the Elder, a Roman naturalist, who described its use in treating liver disease. A hepatoprotective effect is im parted through the flavonoid active ingredient, silymarin. Sily marin alters hepatocyte cell membranes, thereby blocking the toxin-binding sites. Additionally, glutathione, which aids in the detoxification function of the liver, is increased by silymarin. Double-blind, placebo-controlled clinical trials evaluating the efficacy of silymarin on liver function, however, have shown conflicting results. In a study of patients with liver cirrhosis, no difference in survival was found with silymarin compared to placebo (Pares et al., 1998). Another study showed no improvement in cirrhotic liver function after 2 years of treatment; however, benefit was noted in portal hypertension (Ferenci et al., 1989). On the other hand, a significant decrease in liver enzymes was seen with 1 month of silymarin treatment in a group of patients with alcohol-induced liver disease (Salmi & Sarna, 1982). An insignificant de crease in total and conjugated bilirubin was found in the same study.
Numerous changes have been detected in the liver of patients with psoriasis, including steatosis, periportal inflammation, fibrosis, necrosis, and cirrhosis (Pietrzak, Lecewicz-Torun, & Kadziela-Wypyska, 1998). A multifactorial etiology of liver disease in patients with psoriasis has been discussed and includes changes due to alcohol use, nutritional factors, anti-psoriatic medications, and a direct effect of the psoriasis itself. A single case report of clearance of psoriatic arthritis following a portal shunt procedure for primary biliary cirrhosis supports a link (D'Amico, Palazzi, & Capani, 1999). The value of silymarin in the treatment of psoriasis may be due to its ability to improve endotoxin removal by the liver, inhibit cAMP phosphodiesterase, and inhibit leukotriene synthesis. Abnormally high levels of cAMP and leukotrienes have been observed in patients with psoriasis and normalization of these levels may improve the condition (Thorne Research, Inc., 1999). While not proven to directly benefit psoriasis, milk thistle may be of therapeutic value as a hepatoprotective adjunct therapy in patients on hepatotoxic medications.
Cayenne Chilli Pepper, Hot Pepper, Paprika, Red Pepper, Tabasco Pepper (Capsicum annuum, Capsicum frutescens). Cayenne, its chief component being capsaicin, is one of the herbal medicines with documented effectiveness in the English medical literature. One hypothesis on the pathogenesis of psoriasis suggests a neurogenic inflammatory etiology mediated through substance-P (SP). SP activates inflammatory cells and ultimately perpetuates vasodilatation, angiogenesis, and kerat inocyte hyperproliferation (Farber, Nickoloff, Recht, & Fraki, 1986). In accordance, psoriatic lesions are known to be more densely innervated with higher SP content than control or uninvolved psoriatic skin (Naukkarinen, Nickoloff, & Farber, 1989). Capsaicin stimulates the re lease of SP by binding to the vanilloid receptor on slow-conducting, unmyelinated type C neurons and ultimately leads to its depletion.
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