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目的:探讨血管紧张素Ⅱ受体1(AT_1)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AT_1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。
Objective: To investigate the effects of angiotensin Ⅱ receptor 1 (AT_1) and nitric oxide synthase (NOS) on the expression of trx and apoptosis. Methods: Thirty SD rats were randomly divided into sham operation group, AMI group, LOS group, losartan + L-arginine group (LOS + L -NNA), nitro-L-arginine group (L-NNA). AMI model was prepared by ligation of left anterior descending coronary artery. L-NNA inhibits nitric oxide synthase and LOS blocks AT1 receptor. The mRNA expression of Trx, Bcl-2 and Bax in myocardium was semi-quantitatively detected by RT-PCR and the protein expression of Trx was detected by Western blotting. Results: Compared with sham operation group, the expression of Trx mRNA and protein increased, the expression of Bax mRNA increased and the expression of Bcl-2 mRNA decreased in AMI group (P <0.05). Compared with AMI group, Bcl-2mRNA and Trx protein expression increased in LOS group (P <0.05). Compared with AMI group, the mRNA and protein expressions of Trx and the expression of Bcl-2 mR-NA increased in L-NNA group (P <0.05). Compared with LOS group, Bax mRNA, Bcl-2 mRNA and Trx mRNA and protein expression in LOS + L-NNA group were decreased (P <0.05). Compared with LOS + L-NNA group, Bax mRNA, Bcl-2 mRNA, Trx mRNA and protein expression in L-NNA group had no statistical significance. Conclusion: Trx can protect myocardium by antagonizing the apoptosis of myocardial cells in myocardial infarction rats. NOS and AngⅡreceptor signal transduction pathways play an important regulatory role on Trx expression and apoptosis during acute myocardial infarction in rats.