“抗肝纤268方”对肝纤维化的治疗作用

Therapeutic Effect of “Anti-hepatic-fibrosis 268” on Hepatic Fibrosis in Rats

目的 探讨“抗肝纤 2 6 8方”对肝纤维化的影响及机理。方法 制备肝纤维化模型鼠 ,采用“抗肝纤 2 6 8方”高、低剂量治疗 3周 ,对照组用秋水仙碱治疗 ,Masson染色后光镜下统计肝内纤维成分的数量 (IOD值 ) ,免疫组化染色后统计肝内 TGF-β1 、α- SMA、FN、L N、 型胶原、 型胶原等的数量 (IOD值 )。结果 模型组大鼠 FN、L N、 型胶原、 型胶原、TGF- β1 、α- SMA,以及肝内纤维成分等的 IOD值与正常组比较均增高 ,差异有显著性 (P<0 .0 5或 P<0 .0 1 )。“抗肝纤 2 6 8方”低、高剂量以及秋水仙碱治疗 3周后 ,以上指标的 IOD值与模型组比较 ,差异有显著性(P<0 .0 5或 P<0 .0 1 )。低剂量组与高剂量组、对照组比较 ,差异有显著性 (P<0 .0 5 )。结论 “抗肝纤 2 6 8方”可调节 TGF- β1 的数量、进而影响 α- SMA的数量、从而减少细胞外基质 (ECM)数量 。

Objective To investigate the effects of the proprietary Chinese Medicine “anti hepatic fibrosis 268” on hepatic fibrosis and the related mechanisms. Methods The model of CCl 4 induced hepatic damage was established in SD rats. 54 male rats were divided into four groups, namely high dose and low dose “anti hepatic fibrosis 268” groups, colchicine control group, and model control group. Using Masson stain and light microscope, the authors examined the rats' hepatic tissues and counted the hepatic fiber components, then examined and counted TGF β 1, α SMA, FN, Type Ⅰ, Ⅲ collagen by means of immunohistochemical technique. The groups were compared and the internal relationships of the data were analyzed.Results The levels of FN, LN, Type Ⅰ and Ⅲ collagen, TGF β 1, and α SMA of the CCl 4 damaged rats increased ( P <0 01). After 3 weeks of high dose“anti hepatic fibrosis 268” treatment, the levels of TGF β 1, α SMA, FN, LN, Type Ⅰ and Ⅲ collagen decreased ( P <0 01) and the degree hepatic fibrosis took a favorable turn significantly ( P <0 05) as compared with the model control. In the rats of the low dose group, the levels of TGF β 1, α SMA, FN, Type Ⅲ collagen significantly decreased ( P <0.05), the levels of LN, Type Ⅰ collagen were not different from the model control; The hepatic fibrosis improved to a certain extent ( P <0 05). Conclusion The mechanism of reversing hepatic fibrosis by “anti hepatic fibrosis 268” in this experiment is that the medicine regulates TGF β 1 and further affects α SMA, thus resulting in the decline of FN, Type Ⅰ, Ⅲ collagen levels in liver extracellular matrix.