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目的 探讨L- 精氨酸 (L- Arg)对阻塞性黄疸大鼠肝细胞线粒体内Ca2 + 保护作用及其机制。方法 将 72只SD雄性大鼠随机分为对照组 (SO组 ) ,胆总管结扎 +生理盐水组 (BDL +NS组 ) ,胆总管结扎 +L Arg(BDL +L Arg组 )。分别于术后 7、14和 2 1d检测肝细胞线粒体内MDA、SOD、Ca2 + 含量。结果 BDL +NS组各时间点肝细胞线粒体内Ca2 + 、MDA含量明显升高 ,而SOD含量却明显降低。胆总管结扎 7、14d时 ,肝细胞线粒体内Ca2 + 、MDA含量BDL +L Arg组比BDL+NS组低 ,差异有统计学意义 (P <0 .0 1) ;2 1d时 ,肝细胞线粒体内Ca2 + 、MDA含量BDL +NS组和BDL +L Arg中都更进一步升高 ,但两组比较差异无统计学意义(P >0 .0 5 )。胆总管结扎 7d时 ,肝细胞线粒体内SOD含量BDL +L Arg组比BDL +NS组高(P <0 .0 5 ) ;14、2 1d时 ,两组肝细胞线粒体内SOD含量都进一步下降 ,但差异无统计学意义 (P >0 .0 5 )。结论 L Arg在阻塞性黄疸早、中期有保护线粒体作用 ,减少Ca2 + 内流 ,不引起钙超载 ,减轻了阻黄时肝的损伤。
Objective To investigate the protective effect of L-arginine (L-Arg) on mitochondria Ca2 + in hepatocytes of obstructive jaundice rats and its mechanism. Methods 72 SD male rats were randomly divided into control group (SO group), common bile duct ligation + normal saline group (BDL + NS group), common bile duct ligation + L Arg group (BDL + L Arg group). The contents of MDA, SOD and Ca2 + in mitochondria of hepatocytes were detected at 7, 14 and 21 days after operation respectively. Results The contents of Ca2 + and MDA in hepatocytes mitochondria of BDL + NS group were significantly increased at each time point, while the content of SOD was significantly decreased. At 7 and 14 days after common bile duct ligation, the content of Ca2 + and MDA in hepatocyte mitochondria was lower in BDL + L Arg group than in BDL + NS group (P <0.01) The contents of Ca2 +, MDA in BDL + NS group and BDL + L Arg group were all increased further, but there was no significant difference between the two groups (P> 0.05). At 7 days after common bile duct ligation, the content of SOD in hepatocyte mitochondria was higher in BDL + L Arg group than that in BDL + NS group (P <0.05); at 14 and 21 days, SOD content in mitochondria decreased further, But the difference was not statistically significant (P> 0.05). Conclusion L Arg can protect mitochondria in early and middle stages of obstructive jaundice, decrease Ca2 + influx, and do not cause calcium overload, thus reducing liver damage during yellowing.