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作 者:马骏 方以群 包晓辰 王芳芳 李娜[2] 攸璞 张师 陈海庭 Ma Jun;Fang Yiqun;Bao Xiaochen;Wang Fangfang;Li Na;You Pu;Zhang Shi;Chen Haiting(Naval Special Medical Center,Naval Military Medical University,Shanghai 200433,China)
机构地区:[1]海军军医大学海军特色医学中心,上海200433 [2]海军总医院
出 处:《中华航海医学与高气压医学杂志》2020年第3期283-285,共3页Chinese Journal of Nautical Medicine and Hyperbaric Medicine
基 金:全军后勤重大项目(AWS16J033,BWS11J053)。
摘 要: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.
关 键 词:快速上浮脱险 肺损伤 减压病 细胞外调节蛋白激酶
分 类 号:R845.21[医药卫生—航空、航天与航海医学]
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