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目的:本文主要探讨高原低氧对心肌损伤是否通过氧化应激反应机制。方法:将85只大鼠分为高原组和平原组,高原组在海拔4 300m的地区喂养30天,然后取标本。用ELISA方法测量血清或血浆中HIF(低氧诱导因子)、ROS(活性氧)、SOD(超氧化物歧化酶)和CAT(过氧氢酶)的水平,并用West blot方法测定COX-1蛋白表达水平。结果:相比平原组、高原组大鼠血清中HIF-1明显升高,ROS水平显著下降,P<0.000 1,SOD和CAT水平不变或略低,但没有显著性差异;心肌组织中COX-1蛋白表达明显下降,P<0.05。电镜表明心肌细胞线粒体数量减少,水肿,甚至出现结构的破坏。结论:慢性低氧并非通过氧化应激反应引起组织损伤,而是直接性损伤线粒体。
Objective: This article mainly discusses the plateau hypoxia on myocardial injury whether through the oxidative stress response mechanism. Methods: 85 rats were divided into plateau group and plains group. Plateau group was fed for 30 days in the area of 4 300m above sea level, and then specimens were taken. Serum or plasma levels of HIF, ROS, SOD and CAT were measured by ELISA, and the COX-1 protein The expression level. Results: Compared with the plain group, the serum level of HIF-1 was significantly increased and the level of ROS was significantly decreased in the plateau group (P <0.0001). The levels of SOD and CAT were unchanged or slightly lower but not significantly different. The levels of COX -1 protein expression decreased significantly, P <0.05. Electron microscopy showed that the number of mitochondria in myocardial cells decreased, edema, and even structural damage. Conclusion: Chronic hypoxia does not induce tissue injury through oxidative stress, but directly damages mitochondria.