急性心肌梗死再灌注非梗死相关动脉β微管蛋白的表达以及雷米普利干预的实验研究

摘要

Objective:To study expression of β-tubulin in non-infarction related coronary arteries and intervention mechanism of ramipril in rabbits.Methods:Myocardial ischemia-reperfusion model of rabbit was prepared,smooth muscle cells in non-infarction related arteries were divided into 4 groups(10 samples in each group) at random:① hyperlipidemia control group,②myocardium infarction group,③ myocardium infarction reperfusion group,④myocardium infarction reperfusion and ramipril invention group.immunohistochemistry analytical method was used to analysis for β-tubulin in non-infarction related arteries.Expression of β-tubulin in each group was analysised.Results:The thickness of atherosclerotic plaque in myocardium ischemia reperfusion group was more than that in myocardium ischemia group(113.61 ± 25.67) vs.(35.42 ± 11.19) μm(P ＜0.0001),the thickness of atherosclerotic plaque in myocardium infarction reperfusion and ramipril invention group was less than that in myocardium infarction reperfusion group(82.79 ± 17.24)vs.(113.61 ±25.67) μm,P ＜ 0.001),expression of β-tubulin in myocardium infarction reperfusion group was higher than that in myocardium infarction group,(413.61 ± 50.46) vs.(83.15 ± 21.1 2) (P ＜ 0.0001),expression of β-tubulin in myocardium infarction reperfusion and ramipril invention group was lower than that in myocardium infarction reperfusion group (312.79 ± 37.33) vs.(413.61 ± 50.46) (P ＜ 0.0001).Conclusion:Non-infarction related arteries may progress after primary PCI,it may be involved in β-tubulin,ramipril may inhibit progression of non-infarction related arteries by decreasing expression of β-tubulin.%目的:探讨急性心肌梗死后非梗死相关动脉β微管蛋白(β-tubulin)的表达以及雷米普利的干预作用.方法:复制兔高脂血症心肌缺血再灌注模型,分为四组:①高脂血症组,②急性心肌梗死组,③急性心肌梗死再灌注组,④急性心肌梗死再灌注雷米普利干预组.通过荧光免疫组织化学分析方法对各组非梗死相关动脉β微管蛋白行定量分析.结果:缺血再灌注1周后,非梗死相关动脉出现动脉粥样硬化斑块,与急性心肌梗死组及急性心肌梗死再灌注雷米普利干预组相比,急性心肌梗死再灌注组动脉斑块厚度较显著增加(分别P ＜0.0001,P＜0.001);在非梗死相关动脉β微管蛋白表达方面,高脂血症组与急性心肌梗死组差异无统计学意义(P =0.4293),急性心肌梗死再灌注组较急性心肌梗死组显著增加(P ＜0.0001),急性心肌梗死再灌注组较急性心肌梗死再灌注雷米普利干预组显著增加(P＜0.0001).结论:微管蛋白参与心肌缺血再灌注,雷米普利可能通过抑制β微管蛋白表达,延缓非梗死相关动脉病变进展.