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目的探讨N(2)-L-丙氨酰-L-谷氨酰胺(LAG)对肾缺血再灌注致心肌细胞凋亡及相关因子表达的影响。方法清洁级Wistar大鼠30只,体重250~300 g,随机分为3组(n=10):假手术组(sham组)、肾缺血再灌注组(I/R组)和LAG处理组(LAG+I/R组)。Sham组仅切除右肾,游离左肾动脉,关腹。LAG+I/R组和I/R组切除右肾,夹闭左肾动脉45min再灌注以制备肾缺血再灌注模型,分别于夹闭动脉前30min给予LAG150mg/kg和等量生理盐水。三组均于再灌注6h处死大鼠,取心肌组织,HE染色观察病理组织学变化,Masson染色观察心肌细胞变化;ELISA检测血浆中丙二醛(MDA)含量及超氧化物歧化酶(SOD)活性;Western-blot法检测Bcl-2、Bax、Caspase-3蛋白表达水平。结果 N(2)-L-丙氨酰-L-谷氨酰胺能够减轻肾缺血再灌注致心肌细胞损伤,可降低MDA表达水平,升高SOD表达(P<0.05),抑制心肌中Bax和Caspase-3蛋白表达(P<0.05)。结论肾缺血再灌注可导致心肌细胞凋亡,造成一定的心肌损伤,LAG对肾缺血再灌注心脏损伤的保护作用可能与升高SOD和Bcl-2表达,降低MDA、Bax和Caspase-3表达相关。
Objective To investigate the effect of N (2) -L-alanyl-L-glutamine (LAG) on the apoptosis of cardiomyocytes and the expression of related factors during renal ischemia / reperfusion. Methods Thirty Wistar rats, weighing 250-300 g, were randomly divided into 3 groups (n = 10): Sham group, I / R group and LAG group (LAG + I / R group). Sham group only excision of the right kidney, left renal artery free, closed belly. The right kidney was excised from the LAG + I / R group and the left renal artery was occluded for 45 min after reperfusion to prepare a model of renal ischemia / reperfusion. LAG 150 mg / kg and an equal volume of saline were given 30 min before occlusion of the artery. The rats in each group were sacrificed at 6 hours after reperfusion, and the myocardial tissues were harvested. The histopathological changes were observed by HE staining. The changes of myocardial cells were observed by Masson staining. The contents of malondialdehyde (MDA) and superoxide dismutase (SOD) The protein expression levels of Bcl-2, Bax and Caspase-3 were detected by Western-blot. Results N (2) -L-alanyl-L-glutamine decreased the expression of MDA, increased the expression of SOD (P <0.05) and decreased the expression of Bax Caspase-3 protein expression (P <0.05). Conclusion Renal ischemia / reperfusion can induce cardiomyocyte apoptosis and cause myocardial damage. The protective effects of LAG on renal injury induced by ischemia / reperfusion may be related to increasing the expression of SOD and Bcl-2 and decreasing the expression of MDA, Bax and Caspase-3 Expression related.