Effects of Huoxue Chubi Decoction on PDGF-A and TGF-β Expression in Skin of Scleroderma Mice Model / 中国中医药信息杂志

ABSTRACT

Objective To observe the effects of Huoxue Chubi Decoction on contents of PDGF-A and TGF-βin skin lesion of scleroderma mimicking mice models;To discuss its possible mechanism. Methods Thirty mice were randomly assigned into blank group, model group, TCM high-, medium-, low-dose group, with six mice in each group. Other than blank group, the rest of the 4 groups were given bleomycin-hydrocholoride 0.1 mL intradermal injection daily for 3 weeks to establish scleroderma mice models. From week 4 to 7, blank group and model group received gavage with equal amount of distilled water daily;TCM high-, medium-, low dosage group received gavage with Huoxue Chubi Decoction with different concentrations of 44.8, 22.4, 11.2 g/kg daily. The pathological changes in the skin tissue samples taken from each group were observed under microscope;the thickness of skin from each group was measured and the expression of PDGF-A, TGF-β, type-Ⅰ collagen (COL-Ⅰ) and type-Ⅲ collagen (COL-Ⅲ) were tested through immunohistochemical staining. Results Compare with blank group, the dermis tissue of model group was thicker, with the presence of thicker and greater number of collagen fibers, as well as infiltration of inflammatory cells. Compare with model group, thickness of skin and dermis collagen growth of TCM high-, medium-, low-dose group were milder varied by the concentration of the decoction. The result of immunohistochemical staining showed that the expressions of PDGF-A, TGF-β, COL-Ⅰ and COL-Ⅲ of modelgroup significantly increased than blank group (P<0.01); the expression of the mentioned indicators were statistically significant lower in the TCM high-, medium-, low-dose group than model group; The expressions of PDGF-A and TGF-β showed a positive correlation with the amount of COL-Ⅰ and COL-Ⅲpresented in each group. Conclusion Huoxue Chubi Decoction can suppress collagen expression and fibroblast formation in skin lesion of scleroderma mice models by down regulating the expressions of TGF-β and PDGF-A, thus demonstrate its potential in scleroderma treatment.