Apelin通过UCP2减轻缺血再灌注对大鼠肺血管内皮细胞的损伤

The alleviated injury of pulmonary vascular endothelial cells by ischemia-reperfusion by Apelin through UCP2

目的探讨爱帕琳肽(Apelin)对离体肺缺氧复氧损伤的治疗作用及可能机制.方法提取SD乳鼠原代肺上皮细胞,体外建立缺氧复氧模型,分成3组:空白对照组(Con组),缺氧复氧组(AR组),Apelin干预组(Apl组).采用CCK8法检测细胞活力,ELISA法检测白细胞介素-1β(IL-1β)、白细胞介素-6(IL-6)和肿瘤坏死因子-α(TNF-α)的含量以及westernblot法检测解偶联蛋白2(UCP2)的表达.结果Apelin-13能够改善缺氧复氧导致的肺上皮细胞损伤.①细胞活力:AR组<Con组、Apl组(P<0.05).②炎症因子表达:IL-1β含量AR组>Con组、Apl组(P<0.05);IL-6含量AR组>Con组、Apl组(P<0.05);TNF-α含量AR组>Con组、Apl组(P<0.05).③UCP2蛋白表达:AR组<Con组、Apl组(P<0.05).结论缺氧复氧损伤会导致肺上皮细胞活力降低、炎症反应增加和UCP2蛋白表达下降,Apelin-13干预通过上调UCP2蛋白表达控制炎症因子表达,减轻氧化应激反应从而减轻肺上皮细胞缺氧复氧导致的细胞损伤.

Objective To explore the therapeutic effect and possible mechanism of Apelin in the treatment of lung ischemia-reperfusion injury.Methods Primary lung epithelial cells of SD Suckling mice were extracted,and hypoxia and reoxygenation models were established in vitro,and divided into 3 groups:Con group,AR group,and Apelin intervention group(Apl group).Cell activity was detected by CCK8 assay,expression of IL-1β,IL-6 and TNF-α by ELISA and expression of UCP2 protein by Western blot.Results Apelin-13 can ameliorate lung epithelial cell injury caused by hypoxic reoxygenation.①Changes in cell activity:AR group<Con group and Apl group(P<0.05).②Changes in inflammatory factor expression:IL-1β expression:AR group>Con group and Apl group(P<0.05).Changes in IL-6 expression:AR group>Con group and Apl group(P<0.05).Changes in TNF-α expression:AR group>Con group and Apl group(P<0.05).③Changes in UCP2 protein expression:AR group<Con group and Apl group(P<0.05).Conclusion Hypoxic reoxygenation injury can lead to decreased activity of lung epithelial cells,increased inflammatory response and decreased expression of UCP2 protein.Apelin-13 intervention can control the expression of inflammatory factors by upregulating UJCP2 protein expression and reducing oxidative stress response,and thus reduce cell damage caused by hypoxic reoxygenation of lung epithelial ceDs.