快速上浮脱险致减压病早期大鼠肺组织细胞外调节蛋白激酶活性变化研究

来源 :中华航海医学与高气压医学杂志 | 被引量 : 0次 | 上传用户:gfdfh
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目的:探索快速上浮脱险致减压病大鼠肺组织炎性反应机制,观察快速上浮脱险致减压病大鼠发病早期肺组织细胞外调节蛋白激酶(ERK)活性变化。方法:18只大鼠被分为对照组、快速上浮脱险存活组和快速上浮脱险死亡组,每组6只。快速上浮脱险大鼠在不安全的“快速上浮脱险”8 min后麻醉处死取材。所取肺组织应用Western blotting实验检测p-ERK蛋白表达量。结果:快速上浮脱险死亡组大鼠肺组织p-ERK表达量较对照组有显著增高,快速上浮脱险存活组大鼠肺组织p-ERK表达量较对照组无显著增高。结论:快速上浮脱险导致减压病大鼠肺组织发生炎性反应可能与ERK激活有关。“,”Objective:To explore the mechanism of inflammatory response in lung tissues of rats with decompression sickness (DCS) caused by fast buoyancy ascent escape, and to observe the changes in phosphorylation of extracellular signal-related kinase (p-ERK) expression in rats with early onset of DCS during a simulated fast buoyancy ascent escape.Methods:A total of 18 rats were divided into three groups randomly, i. e. control group (C group), escape group in which all six rats were dead (ED group), and escape group in which all six rats survived (ES group). The rats in the ES group were anesthetized and sacrificed 8 minutes after they managed the simulated insecure seawater fast buoyancy ascent escape in a hyperbaric chamber. The p-ERK protein was extracted from rat lungs and then the protein expression was analyzed by Western blotting.Results:The p-ERK expression level in the ED group was elevated significantly than that in the C group; while the p-ERK expression level in ES group was not significantly increased than that in the C group.Conclusion:The development of inflammation-like reaction in lung tissues of rats with DCS caused by fast buoyancy ascent escape may relate with the activation of p-ERK.
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