论文部分内容阅读
目的探讨心肌梗死大鼠心室重塑与还原型烟酰胺腺嘌呤二核苷酸磷酸(NADPH)氧化酶亚单位p22phox和超氧阴离子的关系。方法Sprague-Dawley大鼠冠脉左前降支结扎复制心肌梗死模型,8周后,心脏超声、血流动力学、心脏形态学方法检测分析心室重塑,检测血浆和非梗死心肌脂质过氧化物的浓度。用RT-PCR和免疫组化方法检测p22phox mRNA水平和蛋白水平的分布。用激光共聚焦方法检测心肌超氧阴离子分布。结果心肌梗死后大鼠心室重塑过程显著,与正常对照组比较,左室舒张末压、左室舒张末径[(3.09±1.52vs18.24±6.58)mmHg,(0.67±0.06vs0.90±0.15)mm,P<0.01]和脂质过氧化物水平在血浆和非梗死心肌均显著大于正常对照组(P<0.05)。p22phox mRNA和蛋白表达以及超氧阴离子分布在梗死和非梗死心肌亦均显著增加。结论大鼠心肌梗死后,NADPH氧化酶表达增高,其来源的超氧阴离子可能通过氧化应激参加心室重塑过程。
Objective To investigate the relationship between ventricular remodeling and reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase subunit p22phox and superoxide anion in myocardial infarction rats. Methods Sprague-Dawley rats were ligated and ligated to establish a myocardial infarction model. Eight weeks later, cardiac remodeling was detected by echocardiography, hemodynamics and cardiac morphology. Plasma and non-infarcted myocardium lipid peroxides concentration. The distribution of p22phox mRNA and protein was detected by RT-PCR and immunohistochemistry. Detection of myocardial superoxide anion distribution by laser scanning confocal microscopy. Results Compared with the normal control group, left ventricular end-diastolic pressure, left ventricular end-diastolic diameter [(3.09 ± 1.52vs18.24 ± 6.58) mmHg, (0.67 ± 0.06vs0.90 ± 0.15) mm, P <0.01] and lipid peroxidation levels in plasma and non-infarcted myocardium were significantly greater than those in the normal control group (P <0.05). p22phox mRNA and protein expression and superoxide anion distribution were also significantly increased in infarcted and non-infarcted myocardium. Conclusion The expression of NADPH oxidase increased after myocardial infarction in rats. The superoxide anion derived from it may participate in the process of ventricular remodeling through oxidative stress.