a-硫辛酸对阻塞性黄疸大鼠肝细胞线粒体内能量代谢保护作用及机制

目的 探讨α-硫辛酸对阻塞性黄疸大鼠肝细胞线粒体内能量代谢的保护作用及其机制. 方法 将72只SD雄性大鼠随机分为对照组（SO组）,胆总管结扎＋0.9%氯化钠溶液组（BDL＋NS组）,胆总管结扎α-硫辛酸组（BDL＋LA组）.分别于术后7 d、14 d和2l d检测肝细胞线粒体内MDA、SOD、ATP、ADP和AMP含量并计算总腺苷酸（TAN）和能荷（EC）. 结果 BDL＋NS组各时间点肝细胞线粒体内MDA、ADP、AMP含量明显升高,而SOD、ATP、EC含量却明显降低.胆总管结扎7 d、14 d时,肝细胞线粒体内MDA含量BDL＋LA组比BDL＋NS组低,差异有统计学意义（P＜0.01）;2l d时,AMP、MDA含量BDL＋NS组和BDL＋LA中都更进一步升高,但两组比较差异无统计学意义（P＞0.05）.胆总管结扎7 d、14 d时,肝细胞线粒体内SOD含量、ATP含量BDL＋LA组比BDL＋NS组下降程度有显著性差异（7 d,P＜0.01;14 d,P＜0.05）;21 d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＞0.05）. 结论 α-硫辛酸在阻塞性黄疸早、中期有保护线粒体能量代谢作用,减轻了阻塞性黄疸时肝的损伤.

Protective effect of a-lipoic acid on mitochondrial energy metabolism of liver in the rat with obstructive jaundice

Objective To investigate the effects of α-lipoic acid on mitochondrial energy metabolism of liver in the rat with obstructive jaundice. Methods Seventy-two male SD rats were randomly divided into groups of sham operation and bile duct-ligation ＋ normal soldium（ BDL ＋ NS） and bileduct-ligation ＋ α-lipoic acid（ BDL ＋ LA）. Malondialdehyde（MDA） , superoxide dismutase（SOD） and ATP, ADP, AMP in rat liver＇s mitochondrion were examined on days 7,14,21 after operation. Results MDA contents, ADP contents and AMP contents of liver＇ s mitochondrion were significantly increased at each time point in BDL ＋ NS-group,while SOD contents and ATP contents of liver＇ s mitochondrion decreased remarkably on the 7th, 14th days; MDA content of liver＇ s mitochondrion in BDL ＋ LA group was more lower than that in BDL ＋ NS group （P 〈 0. 01 ）on the 21st day; MDA content was further increased in BDL ＋ NS group and in BDL ＋ LA group but there was no difference in their comparisons. On the 7th, 14th days, SOD contents and ATP contents in BDL ＋ LA group were significantly higher than that in BDL ＋ NS group（ 7th days,P 〈 0. 01; 14th days,P 〈 0.05 ）, On the 21 st day SOD contents in BDL ＋ NS group had no difference with that in BDL ＋ LA group （P 〉 0. 05）. Conclusions LA has a protective effect on energy metabolism of liver＇ s mitochondrion in the initial ,metaphase stage of obstructive jaundice.