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Protection mechanism of early hyperbaric oxygen therapy in rats withpermanent cerebral ischemia

机译:早期高压氧治疗大鼠高血压的保护机制。永久性脑缺血

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摘要

[Purpose] The purpose of this study was to investigate whether early hyperbaric oxygen is useful in rats with permanent cerebral ischemia, and whether its mechanism relates to the inhibition of the tumor necrosis factor-alpha-protein kinase C-alpha pathway. [Subjects] Healthy, male Sprague-Dawley rats (N = 108) were the subjects. [Methods] After middle cerebral artery occlusion models were successfully made, rats were randomly divided into sham-operated, cerebral ischemia, and hyperbaric oxygen groups. At 4 and 12 hours after modeling, the volume of cerebral infarction was determined by triphenyltetrazolium chloride staining, and brain water content was measured using the dry and wet method. The expression of tumor necrosis factor-alpha and protein kinase C-alpha in the ischemic penumbra tissue was measured using Western blot analysis. [Results] The data showed that at 4 and 12 hours after modeling, cerebral infarct volume and brain water content decreased in the hyperbaric oxygen group, and expression of tumor necrosis factor-alpha and phospho-protein kinase C-alpha in the ischemic penumbra tissue also decreased. [Conclusion] Our study demonstrates that early hyperbaric oxygen therapy has protective effects on brain tissue after cerebral ischemia, possibly via inhibition of tumor necrosis factor-alpha and phospho-protein kinase C-alpha.
机译:[目的]研究早期高压氧对永久性脑缺血大鼠是否有用,其机制是否与抑制肿瘤坏死因子-α-蛋白激酶C-α通路有关。 [受试者]健康的雄性Sprague-Dawley大鼠(N = 108)为受试者。方法成功建立脑中动脉闭塞模型后,将大鼠随机分为假手术组,脑缺血组和高压氧组。建模后4小时和12小时,通过氯化三苯基四唑鎓测定脑梗塞的体积,并使用干湿法测量脑含水量。使用蛋白质印迹分析测量缺血性半影​​组织中肿瘤坏死因子-α和蛋白激酶C-α的表达。 [结果]数据显示,在建模后的4和12小时,高压氧组的脑梗死体积和脑含水量降低,缺血半影组织中肿瘤坏死因子-α和磷酸化蛋白激酶C-α的表达。也减少了。 [结论]我们的研究表明,早期高压氧疗法对脑缺血后脑组织具有保护作用,可能是通过抑制肿瘤坏死因子-α和磷酸化蛋白激酶C-α来实现的。

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