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目的探讨烟酰胺腺嘌呤二核苷酸磷酸(NADPH)氧化酶在大鼠心肌梗死后左心室心肌中的改变及夹竹桃麻素对NADPH氧化酶的干预效果。方法 通过结扎雄性SD大鼠左冠状动脉前降支制作大鼠心肌梗死模型,假手术组缝合线只穿过前降支而不结扎。将两组分别随机分为药物干预组和安慰剂组两个亚组[心肌梗死安慰剂亚组(n=7),其余3组(n=6)],术后第2天分别给予等体积夹竹桃麻素[15mg/(kg.d)]和生理盐水灌胃,共5周。术后第6周处死大鼠后取左心室非梗死区心肌组织,采用吸收光度法测定心室肌组织中超氧阴离子(O2-)浓度和NADPH氧化酶活性,采用逆转录多聚酶链反应(RT-PCR)法测定心室肌组织中NADPH氧化酶亚单位gp91phoxmRNA表达水平,并分析心室肌组织中O2-浓度与NADPH氧化酶活性和gp91phoxmRNA表达水平的相关性。结果 心肌梗死组左心室质量、左心室质量指数、心肌组织中O2-浓度、NADPH氧化酶活性及gp91phoxmRNA表达水平均高于假手术组[分别为(746.86±53.09)比(418.33±35.75)mg,2.55±0.34比1.34±0.19,(83200±7582)比(50300±3416)RLU/mg蛋白,(4.77±0.46)比(3.38±0.35)RLU/mg蛋白,0.69±0.06比0.46±0.07,P<0.01或0.05]。心肌梗死药物干预组左心室质量、左心室质量指数、心肌组织中O2-浓度、NADPH氧化酶活性及gp91phoxmRNA表达水平分别为(561.17±81.29)mg、1.91±0.22、(53300±5517)RLU/mg蛋白、(3.62±0.32)RLU/mg蛋白和0.49±0.06,均低于心肌梗死组(均P<0.05)。心肌组织中O2-浓度与NADPH氧化酶活性及gp91phoxmRNA表达水平呈正相关(r值分别为0.76,0.82,均P<0.01)。结论 心肌梗死后心室肌组织中NADPH氧化酶系统被激活,左心室发生重构,左心室质量明显增加,夹竹桃麻素通过抑制NADPH氧化酶活性及其亚单位gp91phoxmRNA的表达而减少心肌组织中O2-生成,从而减轻心肌重构。
Objective To investigate the changes of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase in left ventricular myocardium of rats after myocardial infarction and the effect of apocynin on NADPH oxidase. Methods Myocardial infarction model was induced by ligation of the left anterior descending coronary artery in male SD rats. Sham operation group sutured only through the anterior descending branch without ligation. The two groups were randomly divided into two subgroups: placebo group and placebo group [placebo subgroup of myocardial infarction (n = 7), the other 3 groups (n = 6)], and the same volume Apocynum [15mg / (kg.d)] and saline gavage for 5 weeks. Six weeks after the operation, left ventricular non-infarcted myocardium was sacrificed and the concentration of superoxide anion (O2-) and NADPH oxidase in ventricular myocytes were measured by absorption spectrophotometry. ) Method was used to determine the expression of gp91phox mRNA in ventricular myocytes. The correlation between O2- concentration and NADPH oxidase activity and gp91phox mRNA expression in ventricular myocytes was analyzed. Results Left ventricular mass, left ventricular mass index, myocardial O2-concentration, NADPH oxidase activity and gp91phox mRNA expression in myocardial infarction group were significantly higher than those in sham operation group [(746.86 ± 53.09) vs (418.33 ± 35.75) mg, 2.55 ± 0.34 vs 1.34 ± 0.19, (83200 ± 7582) vs (50300 ± 3416) RLU / mg protein, (4.77 ± 0.46) vs (3.38 ± 0.35) RLU / mg protein, 0.69 ± 0.06 vs 0.46 ± 0.07, P < 0.01 or 0.05]. The levels of left ventricular mass, left ventricular mass index, myocardial O2-concentration, NADPH oxidase activity and gp91phox mRNA expression in myocardial infarction group were (561.17 ± 81.29) mg, 1.91 ± 0.22, (53300 ± 5517) RLU / mg (3.62 ± 0.32) RLU / mg protein and 0.49 ± 0.06, respectively, were lower than those in myocardial infarction group (all P <0.05). The concentration of O2- in myocardial tissue was positively correlated with NADPH oxidase activity and gp91phox mRNA expression (r = 0.76,0.82, all P <0.01). Conclusion NADPH oxidase system is activated in myocardial tissue after myocardial infarction, left ventricular remodeling, left ventricular mass was significantly increased, apocynin through the inhibition of NADPH oxidase activity and its subunit gp91phox mRNA expression decreased myocardial tissue O2- generation, thereby reducing myocardial remodeling.