摘要
目的 :观察胆道梗阻后心肌损伤及川芎嗪 (TMP)的保护作用。方法 :复制大鼠胆道梗阻模型 ,每日予TMP 30mg/kg注射 ,动态观测心肌组织丙二醛 (MDA)和超氧化物歧化酶 (SOD)含量、血清T -Bil、TBA、内毒素 (ET)、肿瘤坏死因子 (TNFα)含量 ;行光电镜检查 ,应用ABC免疫组化染色法 ,定位TNFα在心肌组织中的表达和分布。结果 :胆道梗阻后 ,血清T -Bil、TBA、ET、TNFα水平逐渐升高 ,心肌组织MDA含量逐渐升高 ,SOD逐渐减少 ,各梗阻组与对照组比较 ,P <0 .0 5 ;各TMP治疗组与同时相梗阻组比较 ,血清T -Bil、TBA、ET、TNFα水平下降 (P <0 .0 5 ) ,心肌组织MDA含量减少(P <0 .0 5 ) ,SOD含量升高 (P <0 .0 5 )。结论 :自由基损伤、内毒素血症、TNFα的综合作用是胆道梗阻所致心肌损害的主要机制 。
Objective: To investigate myocardial injury and the protective effects of tetramethylpyrazine (TMP) after biliary obstruction. Methods: The TMP was injected to peritoneum of the rat once a day at a dose of 30 mg/kg after establishment the model of biliary obstruction. The contents of myocardial malondialdyhyde (MDA) and superoxide dismutase(SOD), the levels of serum T-Bil?TBA?endotoxin(ET) ?tumor necrosis factor(TNFα) were determined . Left ventricle myocardium was drawn for optical and electronic microcope observation. Immunohisto-chemical staining method of ABC was to locate the expression and distribution of TNFα in myocardial tissues. Result: After BDL, serum T-Bil?TBA?ET?TNFα levels and myocardium MDA were increased significantly, while SOD decreased markedly as compared with control group (P<0.05); As compared with BDL group at the same obstructed phase, serum T-Bil?TBA?ET? TNFα levels and myocardium MDA in TMP-treated groups were decreased significantly (P<0.05), while myocardium SOD increased significantly (P<0.05). The myocardium MDA content was highly positively correlated with serum TNFα levels. There were less myocardial injuries in TMP-treated groups than those in BDL groups at the same stage by electronic microscopy observation. Conclusion: ET?TNFα and myocardial free radical injury may be the important mechanisms of myocardial injury induced by biliary obstruction; TMP can protect myocardium effectively from the injury after biliary obstruction.
出处
《大连医科大学学报》
CAS
2001年第4期241-243,共3页
Journal of Dalian Medical University
基金
辽宁省教委科研项目 (970 72 2 10 71)
关键词
胆道梗阻
心肌
自由基
肿瘤坏死因子
川芎嗪
biliary obstruction
myocardium
free radical
TNFα
tetramethylpyrazine (TMP)