A hexa-herbal Chinese formula for treatment of atopic dermatitis: phytochemical analysis and selected anti-inflammatory activities

Diverse pharmacological activities and the solid clinical performance of Chinese herbal medicines have attracted worldwide attention in terms of its modernization. Here, a hexaherbal Chinese formula (HHCF) for treating atopic dermatitis (AD) topically has been studied from chemical and biological perspectives. The HHCF comprises the rootstock of Scutellaria baicalensis Georgi (SCU), Rheum tanguticum Maxim. Ex Balf. (RHE), Sophora flavescens Aiton (SOP); the root bark of Dictamnus dasycarpus Turcz. (DIC); the bark of Phellodendron chinense C.K. Schneid. (PHE) and the fruit of Kochia scoparia (L.) Schrad. (KOC). In this thesis the chemical composition of the HHCF has been profiled and characterized using liquid-chromatography (LC) coupled with triple quadruple mass spectrometry (MS). 68 chemical compounds including alkaloids, anthraquinones, coumarins, flavonoids, naphthalene derivatives, phenylbutanone glucosides, phenolic acids, pterocarpans, stilbenes and tannins were putatively identified in the LC-MS profile of the HHCF based on mass measurement and characteristic fragment ions. The source(s) of these chemical compounds has been analyzed using the developed EXCEL template and PHE, RHE and SOP contributed the largest number of chemical compounds identified in the HHCF, while KOC seems to contribute very little. To evaluate the anti-inflammatory effects of the HHCF for treating AD/skin inflammation, the thymus and activation-regulated chemokine (CCL17), Prostaglandin E2 (PGE2), IL-8, IL-6 and hyaluronidase inhibitory effects were studies in vitro. Results showed that the HHCF inhibited hyaluronidase activity, TNF-α- plus IFN--induced CCL17 production in spontaneously immortalized human epidermal keratinocytes (HaCaT) and IL-1β-induced PGE2 in human fibroblasts with no effects on IL-8 and IL- 6. Among the chemical compounds characterized in LC-MS profile of the HHCF, multivariate regression models indicated the major contributor to the CCL17 inhibition were berberine, catechin dimers, gallic acid, galloylglucose, 4-(4'-hydroxylphenyl)-2- butanone 4'-O-β-D-glucoside, pyrogallol and resveratrol 4'-O-β-D-(6''-O-galloyl) glucoside. The effects of the HHCF against other pathogenesis-related targets need to be further study to ascertain its therapeutic efficacy against AD