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作 者:包晓辰 方以群 马骏 王芳芳 BAO Xiao-chen;FANG Yi-qun;MA Jun;WANG Fang-fang(Department of Diving Medicine,Naval Medical Research Institute,Shanghai 200433,China)
机构地区:[1]海军特色医学中心潜水医学研究室,上海200433
出 处:《中国应用生理学杂志》2020年第1期73-76,共4页Chinese Journal of Applied Physiology
基 金:国家自然科学基金项目(81401554)。
摘 要:目的:探讨依达拉奉(edaravone)对肺型氧中毒的保护作用及其机制。方法:30只C57BL/6雄性小鼠,随机分成3组(n=10):空气对照组、高压氧暴露组及依达拉奉预防组,干预组腹腔注射依达拉5 mg/(kg·d),连续3 d后,暴露于2.3 ATA,≥95%氧气中6 h,出舱后收集肺组织,检测肺湿干比。肺组织经苏木素-伊红染色后行病理分析。ELISA检测肺组织中细胞因子、抗氧化酶表达变化。Western检测凋亡基因。结果:依达拉奉注射后可明显减轻高压氧导致的肺损伤,降低肺湿干比,减少细胞因子IL-1β及凋亡蛋白cleaved-caspase3的表达,但对抗氧化酶无明显影响。结论:依达拉奉预防性应用可通过减轻炎症及凋亡对肺型氧中毒起到保护作用。Objective:To find if edaravone can play a protective role in a mouse model of pulmonary oxygen toxicity and explore the intervention mechanism.Methods:Thirty male C57BL/6 mice were randomly divided into 3 groups(Air+Vehicle,Hyperbaric oxygen(HBO)+Vehicle and HBO+Edaravone).Mice were either given edaravone(5 mg/(kg·d))in sterilized water or a sterilized water vehicle for 3 days before oxygen exposure.Mice in HBO groups were exposed to 0.23 MPa hyperoxia(≥95%O 2)for 6 h.Lung tissues were collected and the wet/dry ratio of lung were analyzed.For histologic analysis,lung sections were stained with hematoxylin and eosin(HE).Proinflammatory cytokine levels and antioxidant enzyme activities in lungs were determined by using ELISA kits.The expression levels of pro-apoptosis protein were determined with Western blot analysis.Results:Edaravone treatment could significantly reduce lung permeability,decrease tissue pro-apoptosis protein(cleaved-caspase3)and inflammation(IL-1β).However,edaravone treatment had no effect on antioxidant enzyme activities.Conclusion:These results showed that edaravone treatment had a protective role in pulmonary oxygen toxicity through curbing inflammation and apoptosis.
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