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目的 :初步探讨复方红景天抗肝纤维化的疗效与分子机制。方法 :用 CCl4 皮下注射法诱导 SD大鼠肝纤维化模型 ,同时给予复方红景天颗粒口服进行干预性治疗 ,观察大鼠血清肝纤维化指标、肝组织转化生长因子β1 -(TGF-β1 ) m RNA、α1 ( ) m RNA表达水平及肝组织病理学变化。结果 :口服复方红景天可降低肝纤维化大鼠血清 型前胶原 (PC )、 型胶原 (C )、透明质酸 (HA)水平 ,抑制 TGF-β1 m RNA与α1 ( ) m RNA表达的增加 ,并明显改善大鼠肝组织病理变化 ,TGF-β1 m RNA表达的变化与纤维化指标、αl( ) m RNA表达及肝组织病理学改变呈正相关。结论 :复方红景天可能通过抑制 TGF-β1 m RNA、α1 ( ) m RNA表达从而减少胶原纤维合成等机制有效干预CCl4 诱导的大鼠肝纤维化
Objective: To investigate the efficacy and molecular mechanism of compound Rhodiola anti-fibrosis. METHODS: SD rat liver fibrosis model was induced by subcutaneous injection of CCl4, and compound Rhodiola granules were given orally as an intervention therapy to observe serum hepatic fibrosis indexes and liver tissue transforming growth factor β1 - (TGF-β1 ). m RNA, α1 () m RNA expression levels and histopathological changes in the liver. RESULTS: Oral administration of Rhodiola rosea could reduce the serum levels of procollagen (PC), collagen (C), and hyaluronic acid (HA) in rats with hepatic fibrosis and inhibit the expression of TGF-β1 m RNA and α1 () m RNA. Increased, and significantly improved liver pathological changes in rats, TGF-β1 m RNA expression and fibrosis, αl () m RNA expression and liver pathological changes were positively correlated. Conclusion: Compound Rhodiola may interfere with CCl4-induced rat liver fibrosis by inhibiting the expression of TGF-β1 m RNA and α1( ) m RNA and thus reducing collagen fiber synthesis and other mechanisms