首页> 外文会议>Bioinformatics and Biomedical Engineering , 2009. ICBBE 2009 >Normobaric Hypoxia-induced Brain Damage and Mechanism in Wistar Rat
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Normobaric Hypoxia-induced Brain Damage and Mechanism in Wistar Rat

机译:常压低氧诱导的Wistar大鼠脑损伤及其机制

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To evaluate normobaric hypoxia-induced brain damage and discuss the mechanism in wistar rat brain injury, the water content of brain , brain infarction area ratio , the level of lactic acid and Na+-K+-ATPase activity were detected. The expression of HIF-lalpha was confirmed using immunohistochemistry. Histopathological changes of brain in rat model due to hypoxia were investigated using hematoxylin and eosin stain (HE). Results showed that the levels of lactic acid were positively correlated with the degree of hypoxia which caused a concentration-dependent decrease in total Na+-K+- ATPase activity. Compared with the control group, brain water content of rat model had significant difference under serious hypoxia condition. Brain infarction ratio increased sharply when lactic acid level increased and Na+-K+-ATPase activity decreased obviously. Histopathological examination confirmed that there was a necrotic feature in one single hippocampal gyrus neuron cell. HIF-lalpha (hypoxia induced factor-lalpha) was induced by hypoxia at 6% 02. Expression of HIF-lalpha enhanced the hypoxia adaptation capability of the rat model through regulating the expression of multiple genes. Lactic acid, Na+-K+-ATPase and HIF-lalpha played an important role in brain injury as a possible mechanism.
机译:为了评估常压低氧引起的脑损伤,并探讨wistar大鼠脑损伤的机制,脑中的水含量,脑梗死面积比,乳酸水平和Na + -K + -ATPase活性被检测到。使用免疫组织化学证实了HIF-1α的表达。使用苏木精和曙红染色(HE)研究了缺氧引起的大鼠模型脑的组织病理学变化。结果表明,乳酸水平与缺氧程度呈正相关,导致总Na + -K + -ATPase活性呈浓度依赖性降低。与对照组相比,大鼠模型在严重缺氧条件下的脑含水量具有显着差异。乳酸水平升高,脑梗死率急剧增加,Na + -K + -ATPase活性明显降低。组织病理学检查证实单个海马回神经元细胞中有坏死特征。 HIF-1α(低氧诱导因子-1α)在6%02时被低氧诱导。HIF-1α的表达通过调节多个基因的表达增强了大鼠模型的低氧适应能力。乳酸,Na + -K + -ATPase和HIF-1α在脑损伤中可能起重要作用。

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