Endophilin A2通过调节PTEN/Akt通路对心肌细胞急性缺血损伤的影响  被引量:2

Endophilin A2 attenuates the acute ischemic injury of cardiomyocytes by targeting PTEN/Akt signaling pathway

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作  者:沈焕嘉 莫沁杏 陈玉柳 刘芸 SHEN Huanjia;MO Qinxing;CHEN Yuliu;LIU Yun(Department of Pharmacology,School of Pharmaceutical Science,Guangzhou Medical University,Guangzhou 511436,China)

机构地区:[1]广州医科大学药学院药理教研室,广州511436

出  处:《实用医学杂志》2018年第17期2856-2861,共6页The Journal of Practical Medicine

基  金:广东省科技计划项目(编号:2014A020212607);广州市教育科研项目(编号:1201630448);广州医科大学大学生科技创新项目(编号:2017A082);大学生创新创业训练计划项目(编号:201810570018)

摘  要:目的探讨endophilin A2(EndoA2)对大鼠心肌细胞急性缺血损伤的影响,并初步探讨PTEN/Akt在其中的作用。方法 H9C2心肌细胞转染EndoA2干扰链或过表达腺病毒沉默或过表达EndoA2,再给予氧糖剥夺(OGD)处理,建立心肌细胞急性缺血模型。采用CCK-8法检测细胞存活率;利用Annexin V-FITC/PI双染法检测细胞凋亡情况;使用Western blotting检测凋亡蛋白Caspase-3及PTEN/Akt通路相关蛋白的表达情况。结果 CCK-8和Annexin V-FITC/PI双染结果显示,过表达EndoA2抑制OGD诱导的心肌细胞凋亡,提高心肌细胞存活率,沉默EndoA2则进一步促进OGD诱导的心肌细胞凋亡。Westernblotting结果显示,过表达EndoA2明显抑制OGD诱导的Caspase-3活化,激活PTEN/Akt通路,沉默EndoA2则发挥相反的作用。结论 EndoA2对H9C2心肌细胞急性缺血损伤具有保护作用,其机制可能与激活PTEN/Akt通路有关。Objective To investigate the effect of endophilin A2(EndoA2)on the acute ischemic injury of cardiomyocytes,and to elucidate the role of PTEN/Akt signaling involved.Methods H9C2 cardiomyocytes were treated with oxygen-glucose deprivation(OGD)after transfection with siRNA or the recombinant Ad-EndoA2 adenovirus to decrease or increase EndoA2 expression.CCK-8 assay was performed to detect cell viability,and Annexin V-FITC/PI staining was used to detect cell apoptosis.Western blotting assay was performed to detect Caspase-3 expression and activation of PTEN/Akt signaling.Results EndoA2 overexpression inhibited OGD-induced apoptosis and increased viability of H9C2 cardiomyocytes.EndoA2 knockdown exacerbated H9C2 cardiomyocytes apoptosis after OGD treatment.The level of cleaved Caspase-3 was increased in H9C2 cardiomyocytes after OGD treatment,which could be reversed by EndoA2 overexpression and promoted by EndoA2 knockdown.Furthermore,EndoA2 overexpression activated,while EndoA2 knockdown inactivated PTEN/Akt signaling in H9C2 cardiomyocytes after OGD treatment.Conclusion EndoA2 may protect H9C2 cardiomyocytes against OGD injury through activating of PTEN/Akt signaling.

关 键 词:ENDOPHILIN A2 心肌细胞 氧糖剥夺 凋亡 PTEN/Akt 

分 类 号:R54[医药卫生—心血管疾病]

 

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