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目的:观察马来酸罗格列酮对心肌梗死大鼠血流动力学、梗死面积、心肌细胞凋亡率的影响,研究调节心肌组织过氧化物酶体增殖物激活受体γ(PPARγ)基因表达对大鼠心肌梗死的作用。方法:结扎大鼠左冠状动脉主干制作心肌梗死模型,分为非罗格列酮治疗组(AMIA)和罗格列酮[5mg/(kg.d)]治疗组(AMIB),以假手术组作为对照组,MP-150生理记录仪检测血流动力学变化,HE染色检测梗死面积,流式细胞术检测心肌细胞凋亡率,RT-PCR检测心肌组织PPARγ基因表达,观察罗格列酮对上述指标的影响。结果:①左冠状动脉主干结扎后大鼠心功能下降,与假手术组相比,AMIA组大鼠平均动脉压(MAP)、左室收缩峰压(LVPSP)和左室等容期压力变化的最大速率(±dp/dt max)均明显降低,LVEDP升高[(15.5±2.35)比(4.52±0.57)mmHg,P<0.05].②经罗格列酮治疗14 d后,心梗大鼠左室舒张末期后(LVEDP)较AMIA组明显下降[(10.14±2.28)比(15.5±2.35)mm-Hg,P<0.01],心梗面积减少33%,病理组织学改变较AMIA组明显减轻。③大鼠心肌梗死后心肌细胞凋亡率较假手术组升高21.15倍,经罗格列酮治疗14 d后,心肌细胞凋亡率较AMIA组明显降低[(16.04±2.26)%比(26.44±3.51)%,P<0.01]。④经罗格列酮治疗后,心肌梗死大鼠心肌组织PPARγ基因表达量较AMIA及假手术组明显增加[分别为(2.352±0.159),(1.574±0.196)与(0.491±0.078),P<0.001]。结论:罗格列酮能有效降低大鼠心肌梗死后心肌细胞凋亡,减少心肌梗死面积,这可能与其上调梗死后心肌组织中PPARγ基因表达水平,发挥了PPARγ对心肌细胞及局部血管的保护作用有关。
Objective: To observe the effects of rosiglitazone maleate on hemodynamics, infarct size and myocardial apoptosis in myocardial infarction rats, and to study the regulation of peroxisome proliferator - activated receptor γ (PPARγ) gene Expression of myocardial infarction in rats. Methods: The model of myocardial infarction was established by ligation of the left coronary artery in rats. The rats were divided into non-rosiglitazone group (AMIA) and rosiglitazone (5 mg / (kg · d)] group (AMIB) As a control group, hemodynamic changes were detected by MP-150 physiological recorder, infarction area was detected by HE staining, apoptosis rate of cardiomyocytes was detected by flow cytometry, PPARγ gene expression was detected by RT-PCR, rosiglitazone The impact of the above indicators. Results: ①After the ligation of the left coronary artery, the cardiac function of the rats decreased. Compared with the sham operation group, the mean arterial pressure (MAP), left ventricular systolic pressure (LVPSP) and left ventricular (15.5 ± 2.35) vs (4.52 ± 0.57) mmHg, respectively, P <0.05] .②After 14 days of rosiglitazone treatment, the maximum velocity (± dp / dt max) The left ventricular end diastolic pressure (LVEDP) decreased significantly compared with AMIA group (10.14 ± 2.28 vs 15.5 ± 2.35 mmHg, P <0.01), and the myocardial infarct size decreased by 33% . ③The apoptosis rate of cardiomyocytes after myocardial infarction in rats was 21.15 times higher than that in sham operation group, and the apoptosis rate of cardiomyocytes was significantly lower than that in AMIA group [(16.04 ± 2.26)% vs (26.44 ± 3.51)%, P <0.01]. ④ After rosiglitazone treatment, the expression of PPARγ mRNA in myocardium of myocardial infarction rats were significantly increased compared with AMIA and sham-operated group [(2.352 ± 0.159), (1.574 ± 0.196) and (0.491 ± 0.078), P < 0.001]. CONCLUSION: Rosiglitazone can effectively reduce the myocardial cell apoptosis and reduce the area of myocardial infarction after myocardial infarction in rats, which may be related to its up-regulation of PPARγ gene expression in myocardial tissue after myocardial infarction, which exerts the protective effect of PPARγ on cardiomyocytes and local blood vessels related.