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作 者:杜钢军[1] 王梅[1] 林海红[1] 张硕[1] 姬利延[1] 卢琳琳[1]
机构地区:[1]河南大学药学院药理教研室,河南开封475001
出 处:《河南大学学报(医学版)》2009年第3期170-173,199,共5页Journal of Henan University:Medical Science
基 金:国家重点基础研究发展计划项目(973项目);2006CB705706河南省科技攻关项目(632030200)
摘 要:目的:观察灯盏花素对肝纤维化的保护作用,探讨其可能的作用机制。方法:大鼠肝星型细胞HSC体外培养观察灯盏花素对成纤维细胞增殖、激活及细胞外基质分泌的影响;四氯化碳诱导的大鼠肝纤维化模型检测灯盏花素对肝纤维化的保护作用。结果:灯盏花素体外对大鼠肝星型细胞HSC无直接细胞毒作用,但能抑制TGF-β1促进的HSC增殖、激活及透明质酸(HA)、层粘连蛋白(LN)、Ⅰ型胶原(ColⅠ)分泌。体内灯盏花素能抑制四氯化碳诱导的大鼠血清ALT和AST升高,阻止四氯化碳诱导的大鼠肝脏SOD、POD、CAT降低,并降低肝脏羟哺氨酸、胶原、MDA及TGF-β1含量。结论:灯盏花素有肝纤维化保护作用,其机制可能是通过增加抗氧化防御系统和阻止TGF-β信号实现的。Objective: To observe protective effects of breviscapine against hepatic fibrosis and investigate its possible mechanism. Methods: The effects of breviscapine on cell proliferation, activation and extra- cellular matrix secretion were examined in HSCs in vitro. The rat model of carbon tetraehloride (CCL4)induced hepatic fibrosis was used to assess the protective effect of breviseapine against hepatic fibrosis. Results: In vitro, breviscapine had no cytotoxicity directly on HSCs, however, it could suppress cell proliferation, activation and secretion of hyaluronie acid(HA), laminin(LN) and collagen I (Col I ) induced by TGFβ1 in HSCs. In vivo, breviscapine could prevent serum alanine aminotransferase (ALT), aspartate aminotransferase (AST) from increasing, and superoxide dismutase (SOD), peroxidase(POD) and catalase (CAT) in rats with hepatic fibrosis caused by CCl4 from decreasing. In addition, breviscapine was also able to reduce hepatic hydroxyproline,Collage, malondialdehyde (MDA)and TGF-β1 in hepatic fibrosis rats. Conclusion: Breviscapine had protective effect against hepatic fibrosis, the possible mechanism of which take place in that antioxidative defense activities was enhanced and TGFβsignal was inhibited. Key words: Breviscapine; HSCs; Carbon tetrachloride; Hepatic fibrosis; TGF-β1
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