动脉粥样硬化兔模型血液中乳酸脱氢酶和肌酸激酶的动态分析

目的分析实验性动脉粥样硬化(atherosclerosis, AS)大耳白兔血液中乳酸脱氢酶和肌酸激酶的变化规律.方法建立兔动脉粥样硬化模型,检测模型各阶段血液中各种脂质、AST、ALT、LDH、CK、Bun、Cre等生化指标.结果成功地建立了动脉粥样硬化兔模型;大白兔在喂食高胆固醇饲料4周或12周时,血液中总胆固醇(CHO)和低密度脂蛋白胆固醇(LDL-ch)浓度升高(P<0.05);AST、ALT的活性和Bun、Cre的含量变化差异无显著性(P>0.05);而LDH和CK的活性随着动脉粥样硬化的进程而逐渐升高,变化差异有显著性(P<0.05﹚,ASa组和ASb组的LDH活性分别比对照组升高2.2倍和3.5倍,CK的活性则分别增加2.4倍和7.5倍.VitE组与ASb组比较,LDH和CK的活性都显著下降(P<0.05).结论提示血清LDH和CK的活性升高与动脉粥样硬化的进程相关;VitE可能对血管内皮细胞和平滑肌细胞具有保护作用.

The dynamic analysis of lactate dehydrogenase and creatine kinase in the serum of atherosclerotic model rabbit

Objective To analyze the variability of lactate dehydrogenase and creatine kinase in the serum of atherosclerotic rabbit. Methods The model of atherosclerosis was established. The biochemistry quotas such as lipids, AST, ALT, LDH, CK, Bun and Cre were assayed in the serum of atherosclerotic rabbit of each stage. Results The atherosclerotic rabbit model was established successfully. The concentration of total cholesterol (CHO) and low density lipoprotein cholesterol ( LDL-ch ) in the blood of group Asa (feeding with cholesterol and lard for four weeks) and group Asb (feeding with cholesterol and lard for twelve weeks) increased markedly, and there was significantly statistical difference compared with the contrast group( P <0 05), whereas the activity of alanine aminotransferase(ALT) and aspartate aminotransferase (AST) and the concentration of blood urea nitrogen and creatinine(Cre) was always the same( P >0 05). The activities of lactate dehydrogenase(LDH) and creatine kinase(CK) increased along with the development of atherosclerosis. The activity of LDH in the blood of group Asa and group Asb increased by 2 2 times and 3 5 times respectively compared with that of the contrast group; while the activity of CK increased by 2 4 times and 7 5 times respectively. Conclusion The increase of the activities of LDH and CK in the serum of atherosclerotic rabbit may be well correlated with the development of atherosclerosis. Vitamin E may play an important role in the prevention of atherosclerosis by protecting endothelium and smooth muscle cells in arterial wall from destruction.