【作者】 陈永丰；

【导师】 徐京育；

【作者基本信息】 黑龙江中医药大学 ， 中医内科学， 2009， 硕士

【摘要】 目的观察芪桂益脉灵对急性心肌缺血再灌注大鼠心肌细胞凋亡相关基因Fas、Bcl-2蛋白表达的影响,探讨其心肌保护作用及其机制。方法选取Wistar大鼠70只,雌雄各半,随机分为七组(每组10只)并编号:空白对照组、假手术组、缺血再灌注组、缺血预适应组、消心痛组、芪桂益脉灵低剂量组和芪桂益脉灵高剂量组,采用左冠状动脉穿线结扎法制备大鼠心肌缺血再灌注模型,造模成功后取心尖部组织,用HE染色法光镜下观察凋亡细胞的形态学变化;用免疫组化染色法检测心肌细胞凋亡相关基因Fas、Bcl-2蛋白阳性表达情况。结果1.除假手术组和空白对照组外,其余各组心肌细胞都有不同程度的形态学变化,以缺血再灌注组细胞形态损伤为著。2.芪桂益脉灵高、低剂量组,消心痛组,缺血预适应组与缺血再灌注组比较Bcl-2蛋白表达增高,差异显著(P＜0.05);芪桂益脉灵高剂量组可明显上调Bcl-2蛋白表达,与低剂量组比较差异显著(P＜0.05),与消心痛组比较,两者间无显著差异(P＞0.05)。3.缺血再灌注组Fas蛋白表达最高,与其余各组比较有显著性差异(P＜0.05),芪桂益脉灵组能明显下调Fas蛋白表达,且以高剂量组显著,其作用与消心痛组、缺血预适应组相当,三者间比较差异不显著(P＞0.05)。结论1.芪桂益脉灵可减轻急性心肌缺血再灌注模型大鼠的心肌结构的异常。2.芪桂益脉灵可通过下调Fas基因蛋白表达与上调Bcl-2基因蛋白表达抑制心肌细胞凋亡,具有一定的抗心肌损伤作用。3.芪桂益脉灵调控凋亡基因的作用与缺血预适应组、消心痛组相当,提示其具有药理预适应样心肌保护作用。更多还原

【Abstract】 Objective:To observe the effect of QiGuiYiMaiLing(QGYML) on acute myocardial ischemic -reperfusion in rat cardiac myocyte apoptosis related genes Fas,Bcl-2 protein expression to explore their effects and mechanism of myocardial protection.Methods:The left coronary artery ligation were prepared threading myocardial ischemic -reper -fusion model,Wistar rats with 70,half male and female,were randomly divided into seven groups(n=10) and ID:blank control group,sham-operated group,ischemia- reperfusion group,ischemic preconditioning group,isosorbide dinitrate group,low-dose QGYML and QGYML high-dose group,We observe the morphological changes of apoptotic cells by HE staining in electron microscopy and check cardiomyocyte apoptosis related genes Fas, Bcl-2 protein positive expression by immunohistochemical staining.Results:1.In addition to the sham-operated group and blank control group,the remaining myocytes in each group has a different degree of morphological changes.Especially, ischemic -reperfusion injury group was significant for the cell morphology.2.QGYML high-and low-dose group,isosorbide dinitrate group,ischemic preconditioning group increased significantly than ischemic-reperfusion group Bcl-2 protein expression(P＜0.05);Effects of QGYML high-dose group may significantly increase the expression of Bcl-2 protein,and compared with low-dose group,the result is significantly different(P＜0.05),and compared with isosorbide dinitrate group,there was no significant difference(P＞0.05).3.Ischemic-reperfusion group Fas protein expression is the highest,compared with the other groups,and significantly different(P＜0.05),QGYML significantly reduced its expression,and high-dose group was significant,compared with isosorbide dinitrate group and ischemic preconditioning group,the result is equivalent comparison and among the three were no significant differences(P＞0.05).Conclusion: 1.QGYML can reduce the acute myocardial ischemic-reperfusion rat model of myocardial structural abnormalities.2.QGYML,through reduced expression of Fas gene protein and increased Bcl-2 gene protein expression,inhibited cardiomyocyte apoptosis and has a certain role in anti-myoca rdial ischemia.3.The role of QGYML gene regulation of apoptosis is similar to ischemic preconditioning group and isosorbide dinitrate group,may have its pharmacological preconditioning -like myocardial protection.更多还原