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目的探讨中药单体没食子酸对四氯化碳(CCl4)诱导的大鼠肝纤维化影响及其机制。方法采用CCl4制备大鼠肝纤维化模型,观察没食子酸对大鼠肝功能、超氧化物歧化酶(SOD)、丙二醛(MDA)、L-羟脯氨酸(Hyp)、血清透明质酸(HA)、层粘连蛋白(LN)、III型前胶原(HPCIII)含量影响,观察肝脏显微结构变化。结果与对照组比较,模型组大鼠血清中谷丙转氨酶(ALT)[(342.07±28.03)U/L]、谷草转氨酶(AST)[(532.88±115.55)U/L]、M DA含量[(35.07±11.43)nmol/m L]升高,SOD活力[(147.18±32.27)U/m L]下降,血清中Hyp、HA、LN及HPCIII含量[分别为(49.23±10.87)μg/m L、(161.82±35.24)ng/m L、(46.90±24.52)ng/L、(8.47±1.10)ng/m L]明显升高(P<0.01);与模型组比较,高剂量没食子酸组大鼠血清中ALT、AST活力[分别为(280.63±119.50)、(229.82±51.22)U/L]明显下降,MDA含量[(10.32±3.88)nmol/m L]下降、SOD活力[(230.30±17.56)U/m L]升高,血清中Hyp、HA、LN及HPCIII含量[分别为(26.83±8.23)μg/m L、(103.26±7.16)ng/m L、(11.74±3.69)ng/L、(6.00±0.53)ng/m L]明显下降(P<0.05);病理切片结果表明,没食子酸对CCl4所致大鼠肝纤维化有明显改善作用。结论没食子酸具有明显的保肝、抗肝纤维化作用,其机制可能与其提高机体抗氧化能力有关。
Objective To investigate the effect and mechanism of monomeric gallic acid on hepatic fibrosis induced by carbon tetrachloride (CCl4) in rats. Methods Rat hepatic fibrosis model was induced by CCl4, and the effects of gallic acid on the liver function, SOD, MDA, Hyp, serum hyaluronic acid (HA), laminin (LN) and type III procollagen (HPCIII). The changes of liver microstructure were observed. Results Compared with the control group, the serum levels of ALT, AST and AST in the model group were (342.07 ± 28.03) U / L and (532.88 ± 115.55) U / L, ± 11.43) nmol / m L], while the activity of SOD decreased (147.18 ± 32.27) U / m L], and the levels of Hyp, HA, LN and HPCIII in serum were 49.23 ± 10.87 μg / (P <0.01). Compared with the model group, the levels of serum in the high-dose gallic acid group were significantly higher than those in the model group (161.82 ± 35.24 ng / m L, 46.90 ± 24.52 ng / L, 8.47 ± 1.10 ng / The activity of ALT and AST decreased significantly (280.63 ± 119.50, (229.82 ± 51.22) U / L, MDA content [(10.32 ± 3.88) nmol / m L] and SOD activity (230.30 ± 17.56 U / m L], and the levels of Hyp, HA, LN and HPCIII in serum [(26.83 ± 8.23) μg / m L, (103.26 ± 7.16) ng / m L and (11.74 ± 3.69) ng / 6.00 ± 0.53) ng / m L] significantly decreased (P <0.05). The results of pathological examination showed that gallic acid could significantly improve liver fibrosis induced by CCl4 in rats. Conclusion Gallic acid has obvious effect of protecting the liver and preventing hepatic fibrosis, and its mechanism may be related to its ability to improve the antioxidant capacity of the body.