论文部分内容阅读
目的:研究氮氧自由基HPN对高原缺氧小鼠脑组织中缺氧和凋亡蛋白的影响。方法:将60只小鼠随机分为正常对照组、缺氧模型组、乙酰唑胺组和HPN组,单次腹腔注射给药后,在模拟海拔8 000 m环境停留12 h,检测脑组织中乳酸脱氢酶(LD)含量和乳酸脱氢酶(LDH)活性的变化,HE染色观察脑组织病理学改变,蛋白印迹法检测HIF-1α、VEGF、Caspase-3、Bcl-2和Bax蛋白的表达情况。结果:与正常对照组相比,缺氧模型组中LD含量显著增加,LDH活性显著减低,HIF-1α、VEGF、Caspase-3和Bax蛋白表达增强,Bcl-2蛋白表达和Bcl-2/Bax比值降低。经HPN预处理后能够显著降低高原缺氧小鼠脑组织中LD含量,提高LDH活性,改善脑组织学变化,降低HIF-1α、VEGF、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:HPN能够减轻高原缺氧脑组织损伤,作用机制可能与改善能量代谢,降低机体氧化应激,抑制某些凋亡相关蛋白表达有关。
OBJECTIVE: To study the effects of nitroxyl radical HPN on hypoxia and apoptosis proteins in brain tissue of plateau hypoxia mice. Methods: Sixty mice were randomly divided into normal control group, hypoxia model group, acetazolamide group and HPN group. After a single intraperitoneal injection, the mice were kept in a simulated altitude of 8 000 m for 12 h, Lactate dehydrogenase (LD) and lactate dehydrogenase (LDH) activity were observed. Pathological changes of brain tissue were observed by HE staining. The expressions of HIF-1α, VEGF, Caspase-3, Bcl- Express the situation. Results: Compared with normal control group, the content of LDH and the activity of LDH in hypoxia model group were significantly decreased, while the expressions of HIF-1α, VEGF, Caspase-3 and Bax proteins were increased, the expression of Bcl-2 protein and Bcl-2 / Bax The ratio is lower. Pretreatment with HPN could significantly reduce the LD of brain tissue of plateau hypoxia mice, increase the activity of LDH, improve the histological changes, decrease the protein expression of HIF-1α, VEGF, Caspase-3 and Bax, and increase the protein level of Bcl-2 Expression and Bc1-2 / Bax ratio. CONCLUSION: HPN can reduce the anoxic brain injury in high altitude. The mechanism may be related to improving energy metabolism, reducing oxidative stress and inhibiting the expression of certain apoptosis-related proteins.