姜黄素抑制肝纤维化大鼠脂质过氧化物的生成及肝脏TGF-β1和PDGF的表达

目的： 观察姜黄素对肝纤维化过程中活性氧（ROS）、丙二醛（MDA）的生成及转化生长因子-β₁（TGF-β₁）、血小板源性生长因子（PDGF）表达的影响，探讨姜黄素预防肝纤维化的作用机制。方法: 采用四氯化碳腹腔注射方法，每周3次，共8周制作大鼠肝纤维化模型，同时每只大鼠按每100 g体重分别给予20 mg、10 mg、5 mg姜黄素灌胃处理，每周3次，共8周；设立正常组、肝纤维化组和阳性对照组。8周后处死大鼠，留取大鼠肝脏和血清。比色法检测血清ROS水平；硫代巴比妥酸（TBA）法检测肝组织匀浆中MDA含量；免疫组化方法检测各组大鼠肝组织中TGF-β₁、PDGF的表达水平。结果: 模型组大鼠血清ROS水平明显升高，姜黄素可显著降低ROS水平（P＜0.05）；姜黄素组大鼠肝组织中MDA含量明显低于模型组（P＜0.01）；模型组大鼠肝组织中TGF-β₁、PDGF大量表达，姜黄素可明显抑制上述因子的表达（P＜0.01）。结论: 姜黄素可抑制肝脏脂质过氧化物的形成以及TGF-β₁和PDGF的表达，从而发挥预防肝纤维化的作用。

Curcumin inhibits lipid peroxidation and the expression of TGF - β1 and PDGF in the liver of rats with hepatic fibrosis

AIM: To investigate changes of the level of reactive oxygen species (ROS),malondialdehyde (MDA),transforming growth factor-β1 (TGF-β1) and platelet-derived growth factor (PDGF) expression in a rat hepatic fibrosis model and the effect of curcumin ,and discuss the mechanism of the prophylactic effect of curcumin on hepa tic fibrosis.METHODS: Rat models of hepatic fibrosis were established by intraperitoneally injection of carbon tetrachloride.Curcumin of 20 mg,10 mg,5mg per 100 gram weight of rat was given to these rats respectively at the same time.Normal,fibrosis model and positive groups were made as controls.After eight weeks,all rats were executed and the blood and liver were kept.Serum level of ROS was tested by chromatometry.Content of MDA in liver homogenate was tested by thiobarbituric acid (TBA) method.Expressions of TGF-β1 and PDGF in liver were detected by immunohistochemical method. RESULTS: Serum level of ROS in fibrotic group increased significantly compared with that of normal group,and which was depressed obviously in curcumin groups(P＜0.05).Content of MDA in liver of curcumin group reduced significantly compared with that of fibrotic group (P＜0.01).Expressions of TGF-β1 and PDGF in fibrotic group increased significantly compared with those of normal group,which were depressed obviously in curcumin groups (P＜0.01).CONCLUSION: Curcumin could inhibit expression of TGF-β1,PDGF and lipid peroxidation in liver.These may be mechanisms of curcumin preventing hepatic fibrosis.