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目的研究氮氧自由基(nitronyl nitroxide)对高原缺氧小鼠心肌组织缺氧和凋亡蛋白的影响。方法将48只小鼠随机分为正常对照组、缺氧模型组、乙酰唑胺组和氮氧自由基组,单次腹腔注射给药30 min后,在模拟海拔8 000 m环境停留12 h,测定心肌组织中乳酸(LD)含量和乳酸脱氢酶(LDH)活性,Western blotting检测缺氧诱导因子-1α、血管内皮生长因子、caspase-3、Bcl-2和Bax蛋白的表达水平。结果与正常对照组相比,缺氧模型组中乳酸含量和乳酸脱氢酶活性显著增加,缺氧诱导因子-1α、血管内皮生长因子、caspase-3和Bax蛋白表达增强,Bcl-2蛋白的表达和Bc1-2/Bax比值降低。经氮氧自由基预处理后能够显著降低高原缺氧小鼠心肌组织中乳酸含量和乳酸脱氢酶活性,降低缺氧诱导因子-1α、血管内皮生长因子、caspase-3和Bax蛋白表达,提高Bcl-2的蛋白表达和Bc1-2/Bax比值。结论氮氧自由基对高原缺氧诱导的心肌组织损伤具有保护作用,该作用可能其与改善能量代谢、降低机体氧化应激及抑制心肌细胞凋亡等作用有关。
Objective To investigate the effect of nitronyl nitroxide on hypoxia and apoptosis protein in cardiac muscle of plateau hypoxia mice. Methods 48 mice were randomly divided into normal control group, hypoxia model group, acetazolamide group and nitroxide group. After a single intraperitoneal injection for 30 min, the mice were maintained in a simulated altitude of 8 000 m for 12 h, Lactate (LD) and lactate dehydrogenase (LDH) activity in myocardium were measured. The expression of HIF-1α, VEGF, caspase-3, Bcl-2 and Bax protein were detected by Western blotting. Results Compared with the normal control group, the content of lactate and the activity of lactate dehydrogenase in hypoxia model group were significantly increased, while the expression of hypoxia inducible factor-1α, vascular endothelial growth factor, caspase-3 and Bax protein increased, while the expression of Bcl-2 protein The expression and Bc1-2 / Bax ratio decreased. Nitroxide preconditioning can significantly decrease the content of lactate and lactate dehydrogenase in myocardial tissue of hypoxic mice and decrease the expression of hypoxia inducible factor-1α, vascular endothelial growth factor, caspase-3 and Bax Bcl-2 protein expression and Bc1-2 / Bax ratio. Conclusion Nitrogen and oxygen free radicals may have a protective effect on myocardial injury induced by plateau hypoxia, which may be related to improving energy metabolism, reducing oxidative stress and inhibiting cardiomyocyte apoptosis.