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机构地区:[1]广州医学院从化学院药理教研室,广州市510925
出 处:《医学理论与实践》2005年第10期1133-1135,共3页The Journal of Medical Theory and Practice
摘 要:目的:观察硝苯啶抗大鼠肝纤维化的疗效。方法:80只Wistar大鼠随机分为早期治疗组和晚期治疗组,每组又分为大、中、小剂量组、模型组和正常组。免疫组化法检测大鼠肝组织中血小板源性生长因子-BB(PDGF-BB);肝组织HE染色观察病理变化。结果:与模型组相比,硝苯啶早期治疗组和晚期治疗组大鼠肝组织中PDGF-BB表达明显减少(P<0.05),肝组织病理改变明显减轻。结论:硝苯啶能有效防治大鼠肝纤维化的肝损伤和纤维化形成,其机制可能与硝苯啶阻断钙离子通道,抑制PDGF介导的HSC增殖有关。Objective: To investigate the effect and mechanism of nifedipine on PDGF- BB in fibrofic liver in rats. Methods:80 Wistar rots were randomly divided into two groups: early and late treated with nifedipine group, then each group was divided into five groups: low, median, high dose ,model and control group respectively(each group, n = 8) .The effect of nifedipine on the level of platelet - derived growth factor(PI)GF) - BB was evaluated by immunohistochemical assay. The liver histopathology was also examined by HE staining. Results:Compared with the model group, the contents of PDGF- BB were significantly decreased in all therapeutic groups (P 〈 0.05);and the histopathology changes were also obviously improved in treated rats. Conclusion: Nifedipine has protective and therapeutic effects on liver injure and can inhibit hepatic fibrosis induced by CCl4 in rats. Its mechanism may be associated with its effect of block Calcium channel, and suppressing the activation of hepatic stellate cells induced by PDGF- BB.
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