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Effects of oxymatrine on experimental hepatic fibrosis and its mechanism in vivo.

机译:氧化苦参碱对实验性肝纤维化的影响及其体内机制。

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AIM: Hepatic fibrogenesis has close relation with hepatic stellate cells (HSC) and tissue inhibitors of metalloproteinase (TIMP). Oxymatrine (OM) is a kind of Chinese herb that is found to have some effects on liver fibrosis. We aimed to determine the effects of OM on hepatic fibrosis and explore the possible mechanism. METHODS: Thirty-two rats were randomly divided into four groups; 16 were used to develop hepatic fibrosis by carbon tetrachloride (CCl4) and treated with or without OM, and 16 were used as controls. The expression of tissue inhibitor of metalloproteinase-1 (TIMP-1) and alpha-smooth muscle actin (alpha-SMA) in the livers of rats was detected by immunohistochemical assay. Liver pathology was determined by H and E staining and reticulum staining. RESULTS: In CCl4-injured rats, the normal structure of lobules was destroyed, and pseudolobules were formed. Hyperplasia of fibers was observed surrounding the lobules. While the degree of fibrogenesis in liver tissues was significantly decreased in those rats with OM-treatment compared with those without OM treatment. The pseudolobules were surrounded by strong, multi-layer reticular fibers, which netted into pseudolobules in CCl4-injured rats, however, there was a significant decrease in reticular fibers in OM-treated rats. The expression of TIMP-1 in hepatic cells was weak in control groups, but strong in CCl4-injured groups, however, the expression of TIMP-1 was significantly inhibited by OM (F = 52.93, P<0.05). There was no significant change in the expression of alpha-SMA between CCl4-injured rats with or without OM treatment (F = 8.99, P>0.05). CONCLUSION: OM effectively inhibits CCl4-induced fibrogenesis in rat liver tissues, probably by reducing the expression level of TIMP-1.
机译:目的:肝纤维化与肝星状细胞(HSC)和金属蛋白酶组织抑制剂(TIMP)密切相关。氧化苦参碱(OM)是一种中草药,被发现对肝纤维化有一定作用。我们旨在确定OM对肝纤维化的影响并探讨可能的机制。方法:32只大鼠随机分为4组。 16例通过四氯化碳(CCl4)发生肝纤维化,并在有或无OM的情况下进行治疗,另外16例用作对照。免疫组织化学法检测大鼠肝脏中金属蛋白酶-1(TIMP-1)和α-平滑肌肌动蛋白(alpha-SMA)的组织表达。通过H和E染色和网状染色确定肝脏病理。结果:在CCl4损伤的大鼠中,小叶的正常结构被破坏,并形成假小叶。在小叶周围观察到纤维增生。与未进行OM处理的大鼠相比,进行OM处理的大鼠肝脏组织中的纤维形成程度明显降低。假小叶被结实的多层网状纤维包围,在CCl4损伤的大鼠中网状进入假小叶,但是在OM处理的大鼠中,网状纤维明显减少。肝细胞中TIMP-1的表达在对照组中较弱,而在CCl4损伤组中较强,然而,OM显着抑制了TIMP-1的表达(F = 52.93,P <0.05)。在有或没有进行过OM处理的CCl4损伤的大鼠之间,α-SMA的表达没有显着变化(F = 8.99,P> 0.05)。结论:OM可能通过降低TIMP-1的表达水平来有效抑制CCl4诱导的大鼠肝组织纤维化。

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