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赵川, 李俊萱, 陈山琼, 韦燕飞. 没食子酸抗实验性肝纤维化作用机制[J]. 中国公共卫生, 2016, 32(11): 1498-1501. DOI: 10.11847/zgggws2016-32-11-13
引用本文: 赵川, 李俊萱, 陈山琼, 韦燕飞. 没食子酸抗实验性肝纤维化作用机制[J]. 中国公共卫生, 2016, 32(11): 1498-1501. DOI: 10.11847/zgggws2016-32-11-13
ZHAO Chuan, LI Jun-xuan, CHEN Shan-qiong.et al, . Effect of gallic acid on experimental liver fibrosis in rats[J]. Chinese Journal of Public Health, 2016, 32(11): 1498-1501. DOI: 10.11847/zgggws2016-32-11-13
Citation: ZHAO Chuan, LI Jun-xuan, CHEN Shan-qiong.et al, . Effect of gallic acid on experimental liver fibrosis in rats[J]. Chinese Journal of Public Health, 2016, 32(11): 1498-1501. DOI: 10.11847/zgggws2016-32-11-13

没食子酸抗实验性肝纤维化作用机制

Effect of gallic acid on experimental liver fibrosis in rats

  • 摘要: 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、MDA含量(35.07±11.43)nmol/mL升高,SOD活力(147.18±32.27)U/mL下降,血清中Hyp、HA、LN及HPCⅢ含量分别为(49.23±10.87)μg/mL、(161.82±35.24)ng/mL、(46.90±24.52)ng/L、(8.47±1.10)ng/mL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/mL下降、SOD活力(230.30±17.56)U/mL升高,血清中Hyp、HA、LN及HPCⅢ含量分别为(26.83±8.23)μg/mL、(103.26±7.16)ng/mL、(11.74±3.69)ng/L、(6.00±0.53)ng/mL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。

     

    Abstract: Objective To explore the effect of gallic acid (GA) on carbon tetrachloride (CCl4)-induced hepatic fibrosis in rats and its mechanism.Methods The rat hepatic fibrosis model was established with CCl4,and then the rats were treated witn GA.The changes in hepatic function,blood hyaluronic acid (HA),superoxide dismutes (SOD),malondialdehyde (MDA),L-hydroxyproline (Hyp),serum HA,laminin (LN),and procollagen type Ⅲ (HPCⅢ)were detected and the changes in microstructure of hepatic tissues were also observed.Results Compared with those of the normal control group,the serum alanine transaminase (ALT)(342.07±28.03 U/L),aspartate aminotransferase (AST)(532.88±115.55 U/L),MDA (35.07±11.43 nmol/mL),Hyp (49.23±10.87μg/mL),HA (161.82±35.24 ng/mL),LN (46.90±24.52 ng/L),and HPCⅢ (8.47±1.10 ng/mL)of the model group were increased significantly (P<0.01 for all);while the serum SOD (147.18±32.27 U/mL) was decreased (P<0.01).Compared with those of the model control group,the ALT (280.63±119.50 U/L),AST (229.82±51.22 U/L),MDA (10.32±3.88 nmol/mL),Hyp (26.83±8.23μg/mL),HA (103.26±7.16 ng/mL),LN (11.74±3.69 ng/L), and HPCⅢ (6.00±0.53 ng/mL) of the high dose GA group were decreased significantly (P<0.01 for all);while the activity of SOD (230.30±17.56 U/mL) was increased (P<0.01).The pathological observation revealed that GA could improve injuries of hepatic tissues.Conclusion GA has the effects of protecting liver and anti-liver fibrosis and the mechanism of the effects may be related to its anti-oxidation role.

     

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