This study was first and systematically conducted to evaluate the hypoxia response of the brain, heart, lung, liver, and kidney of mice exposed to an animal hypobaric chamber. First, we examined the pathological damage of the above tissues by Hematoxylin & eosin (H&E) staining. Secondly, biochemical assays were used to detect oxidative stress indicators such as superoxide dismutase (SOD), malondialdehyde (MDA), reduced glutathione (GSH), and oxidized glutathione (GSSG). Finally, the hypoxia compensation mechanism of tissues was evaluated by expression levels of hypoxia-inducible factor 1 alpha (HIF-1α), erythropoietin (EPO), and vascular endothelial growth factor (VEGF). During the experiment, the mice lost weight gradually on the first 3 days, and then, the weight loss tended to remain stable, and feed consumption showed the inverse trend. H&E staining results showed that there were sparse and atrophic neurons and dissolved chromatin in the hypoxia group. And hyperemia occurred in the myocardium, lung, liver, and kidney. Meanwhile, hypoxia stimulated the enlargement of myocardial space, the infiltration of inflammatory cells in lung tissue, the swelling of epithelial cells in hepatic lobules and renal tubules, and the separation of basal cells. Moreover, hypoxia markedly inhibited the activity of SOD and GSH and exacerbated the levels of MDA and GSSG in the serum and five organs. In addition, hypoxia induced the expression of HIF-1α, EPO, and VEGF in five organs. These results suggest hypoxia leads to oxidative damage and compensation mechanism of the brain, heart, lung, liver, and kidney in varying degrees of mice.

中文翻译：

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低压缺氧小鼠多器官损伤及代偿机制


这项研究首次系统地评估了暴露于动物低压室的小鼠的大脑、心脏、肺、肝脏和肾脏的缺氧反应。首先，我们通过苏木精和伊红（H&E）染色检查上述组织的病理损伤情况。其次，通过生化检测检测氧化应激指标，如超氧化物歧化酶（SOD）、丙二醛（MDA）、还原型谷胱甘肽（GSH）和氧化型谷胱甘肽（GSSG）。最后，通过缺氧诱导因子1α（HIF-1α）、促红细胞生成素（EPO）和血管内皮生长因子（VEGF）的表达水平评估组织的缺氧补偿机制。实验过程中，小鼠体重在前3天逐渐下降，之后体重下降趋于稳定，饲料消耗量呈相反趋势。 H&E染色结果显示，缺氧组神经元稀疏、萎缩，染色质溶解。心肌、肺、肝、肾均出现充血。同时，缺氧刺激心肌间隙扩大，肺组织炎性细胞浸润，肝小叶、肾小管上皮细胞肿胀，基底细胞分离。此外，缺氧显着抑制了血清和五脏器中SOD和GSH的活性，升高了MDA和GSSG的水平。此外，缺氧还诱导五个器官中HIF-1α、EPO和VEGF的表达。这些结果表明缺氧导致小鼠不同程度的脑、心、肺、肝、肾氧化损伤和代偿机制。