摘要
目的探究洛伐他汀预处理对急性心脏缺血再灌注心肌细胞凋亡的影响。方法将24只SD大鼠随机均分为3组模型对照组(C);洛伐他汀(Lovastatin)组(L),胃管直接灌注洛伐他汀每天15mg/kg,2周;洛伐他汀L-硝基精氨酸甲酯(L-NAME)组(N),洛伐他汀每天15mg/kg直接灌胃同时腹腔注射L-NAME30mg/kg,2周。2周后建立在体急性缺血再灌注心脏模型,观察洛伐他汀对缺血再灌注前、后心肌细胞Bcl-2、Bax凋亡相关蛋白表达以及心肌细胞凋亡的影响。结果各组血脂指标差异无统计学意义,洛伐他汀上调心肌细胞内Bax凋亡相关蛋白表达(P<0.05),对Bcl-2凋亡相关蛋白影响不明显(P>0.05);明显降低缺血再灌注心肌细胞凋亡指数(P<0.05)。结论洛伐他汀有效减少心脏缺血再灌注后心肌细胞凋亡,具有非降脂的延迟性心肌保护作用。其抗凋亡作用不受抑制一氧化氮合酶(NOS)活性和改变心肌细胞内凋亡相关蛋白Bax表达影响,具体机制须进一步实验探究。
Objective To study the effects and mechanisms of Lovastatin preconditioning on cardiac myocyte apoptosis in acute ischemic and reperfused （I/R） rat hearts. Methods 24 Sprague-Dawley male rats were randomly divided into three groups： control group （C）; Lovastatin group （L） treated with lovastatin 15 mg/kg once a day for two weeks; Lovastafin and L-NAME group （N） treated with the same dose of Lovastatin with L group and L-NAME 30 mg/kg once a day for two weeks. Rat heart models of I/R were established with coronary occlusion 30 mintues and reperfusion 30 mintues of the left anterior descending artery, after two-week administration. Expression of Bcl-2,Bax protein and myocardium apoptosis were investigated in every group, Results There was no change in blood lipin, expression of Bax protein was increased （P 〈 0.05 ） and the index of myocyte apoptosis （AI） was significantly lower （ P 〈 0.05）, but expression of Bcl-2 protein was not changed in the L group. Conclusion Lovastatin can protect the heart from ischemic and reperfusied injury by decreasing myocardiocyte apoptosis. Lovastatin may have delayed protective effect on the ischemic and reperfused rat myocardium, but such effects didn＇t correlate to its effect on lipin in blood serum.
出处
《中华胸心血管外科杂志》
CSCD
北大核心
2005年第5期289-291,共3页
Chinese Journal of Thoracic and Cardiovascular Surgery
