中文摘要：

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。

英文摘要：

OBJECTIVE To evaluate effects of HNP on expression of hypoxia and apoptosis associated proteins in heart of mice during hypobaric hypoxia. METHODS Sixty BALB/C mice were randomly divided into normal control group, hypoxia model group, acetazolamide group and HPN group. After single intraperitoneal injection, mice were exposed to hypobaric hy- poxia （8 000 m） for 12 h. Lactate（LD） level and lactate dehydrogenase（LDH） activity in heart were monitored. Brain tissue sections were examined by hematoxylin and eosin （HE） staining. Expression levels of HIF-1α, VEGF, Caspase-3, Bcl-2 and Bax were determined by Western blotting. RESULTS Content of LD in hypoxia model group significantly increased while LDH activity markedly decreased compared with normal control group. Hypobaric hypoxia exposure signicantly upregulated expression levels of HIF-1α, VEGF, Caspase-3 and Bax as well as reduced Bcl-2 expression and Bcl-2/Bax ratio. Prior adminis- tration of HPN appreciably attenuated tissue lesion of heart, decreased LD levels and expression of HIF-lα, VEGF, Caspase-3 and Bax and increased LDH activity, Bcb2 expression and Bcl-2/Bax ratio. CONCLUSION Protection of HPN against hypo- baric hypoxia-indueed heart injury can be explained in part by amelioration of energy metabolism, alleviation of oxidative stress as well as inhibition of some apoptosis protein.