【摘要】 目的:探讨血管紧张素Ⅱ受体1（AT₁）和一氧化氮合酶（NOS）对硫氧还蛋白（Trx）表达及细胞凋亡的影响。方法:SD大鼠30只,完全随机分组:假手术组（sham）、急性心肌梗死组（AMI）、氯沙坦组（LOS）、氯沙坦+硝基左旋精氨酸组（LOS+L-NNA）、硝基左旋精氨酸组（L-NNA）。用结扎冠状动脉左前降支法制备AMI模型。L-NNA抑制一氧化氮合酶,LOS阻断AT₁受体。RT-PCR半定量检测心肌Trx、Bcl-2、Bax mRNA表达,Western blotting检测Trx蛋白表达。结果:AMI组与假手术组相比较,Trx mRNA及蛋白表达增加,Bax mRNA表达增强,Bcl-2 mRNA表达降低（P<0.05）。LOS组与AMI组相比较Bcl-2mRNA,Trx蛋白表达增加（P<0.05）。L-NNA组与AMI组相比较,Trx mRNA及蛋白表达降低,Bcl-2 mR-NA表达增加（P<0.05）。LOS+L-NNA组与LOS组相比较Bax mRNA、Bcl-2 mRNA、Trx mRNA及蛋白表达均降低（P<0.05）。L-NNA组与LOS+L-NNA组相比较,Bax mRNA、Bcl-2 mRNA、Trx mRNA及蛋白表达差异无统计学意义。结论:Trx在心肌梗死大鼠中通过拮抗心肌细胞凋亡而对心肌起保护作用。大鼠急性心肌梗死过程中NOS和AngⅡ受体信号转导通路对Trx表达及细胞凋亡有重要的调节作用。更多还原

【Abstract】 Objective:To investigate the regulatory effects of nitric oxide synthase(NOS) and angiotensinⅡ(AngⅡ) on expression of thioredoxin(Trx) and cardiomyocyte apotosis in rats with actute myocardial infarction(AMI).Methods:Thirty SD rats were randomly divided into 5 groups(n = 6 each):the sham operation group(sham),the AMI group,the losartan group(LOS),the losartan + N-nitro-L-arginine group(LOS + L-NNA),the N-nitro-L-arginine group(L-NNA).The left anterior descending branch of coronary artery was ligated to develop AMI model.L-NNA was used to inhibit the NOS,as was LOS to block the AT,receptor.RTPCR was employed to detect the Trx mRNA,Bax mRNA,Bcl-2 mRNA in myocardium.Thioredoxin was measured by Western blotting analysis.Results:The levels of Bax mRNA,Trx mRNA and Trx protein expression were elevated,while the level of Bcl-2 mRNA was lower in AMI group than in sham group(all P<0.05 ).Compared with AMI group,the levels of Bcl-2 mRNA and Trx protein expression were higher in LOS group.The levels of Trx mRNA and protein expression were lower,while Bcl-2 mRNA expression was higher in L-NNA group than in AMI group(all P<0.05 ).The levels of Bax mRNA,Bcl-2 mRNA,Trx mRNA and protein expression were lower in LOS + L-NNA group than in LOS group(all P<0.05 ).Conclusion:Thioredoxin plays important role against cardiomyocyte apotosis in AMI rats.During acute myocardial infarction,nitric oxide synthase and angiotensinⅡtype 1 receptor signaling pathway may have a critical role in regulating Trx expression and myocyte apotosis.更多还原