【摘要】 目的:观察鬼针草总黄酮(totalflavonesofBi-denspilosaL,TFB)的抗肝纤维化作用。方法:将大鼠随机分为六组:正常对照组,模型组,TFB160、80、40mg.kg-1组和秋水仙碱0.1mg.kg-1阳性药对照组。除正常对照组外,其余各组采用皮下注射四氯化碳(CCl4)诱导肝纤维化模型。于造模第9周起,给药组分别灌胃相应的受试药物,正常对照组和模型组灌胃等容量的生理盐水,疗程10周。实验结束后,取大鼠血清测ALT、AST、透明质酸(HA)、Ⅲ型前胶原肽(PCⅢ)、Ⅳ型前胶原酶(CⅣ);取大鼠肝、脾称重,计算肝、脾指数;同时取固定部位肝组织,测定组织中MDA、Hyp含量和GSH-Px活性;另取部分肝组织做病理组织学和电镜学检查。结果:TFB160、80mg.kg-1能显著降低肝纤维化大鼠肝、脾指数,并降低血清中ALT、AST活性及HA、PCⅢ、CⅣ和肝组织中MDA、Hyp含量,且升高肝组织中GSH-Px活性(P<0.05)。病理组织学和电镜检查结果显示TFB160、80mg.kg-1组肝脏组织结构明显改善,肝纤维化增生程度减轻。结论:TFB对CCl4所致大鼠肝纤维化有明显治疗作用,其机制可能与抑制氧自由基的生成有关。更多还原

【Abstract】 AIM: To observe the curative effect of total flavones of Bidens pilosa L （TFB） on experimental liver fibrosis in rats. METHODS: Rat liver fibrosis model was established by subcutaneous injection （ s.c. ） of 50% CCl₄ twice a week lasting for 18 weeks. TFB （160, 80, 40 mg·kg -1 ） was treated gastrogavage （ i.g. ） daily since the 9th week. The spleen and liver weights were weighed. The contents of alanine aminotransferase （ALT）, aspartate aminotransferase （AST）, hydroxyproline （Hyp）, malondialdehyde （MDA） and glutathione peroxidase （GSH-Px） in liver tissue were assayed using the corresponding kits. The hyaluronic acid （HA）, procollagen III （PCⅢ） and CⅣcontents in serum were also assessed by radioimmunoassay. Liver samples collected after experiment were stained with hematoxylin-eosin （HE） and Masson and scored. Moreover, electron microscope was used to observe ultramicrosrtucture of the cells in livers. RESULTS: CCl₄ caused liver fibrosis, featuring increases in spleen and liver weights,serum ALT, AST, HA , PCⅢ, CⅣ, and liver MDA and Hyp contents, a decrease in liver GSH-Px activity. Compared with model group, TFB （160, 80 mg·kg -1 ） treatment significantly reduced spleen and liver weight, serum ALT, AST, HA , PCⅢ, CⅣ, liver MDA and Hyp content （P< 0.01 ）. Moreover, TFB 160 or 80 mg·kg -1 could increase liver GSH-Px activity （P< 0.01 ）. Fibrosis changes of liver histology was also improved in TFB （80, 160 mg·kg -1 ）-treated rats （P< 0.05 ）. CONCLUSION: TFB significantly reduced CCl₄-induced liver fibrosis in rats, probably through exerting a protective effect by its free-radical scavenging ability.更多还原