中国药理学通报2017，Vol.33Issue(7)：971-976,6.DOI:10.3969/j.issn.1001-1978.2017.07.017
PI3K/Akt/FoxO3a/Bim信号通路介导硫化氢后处理对缺氧H9c2心肌细胞的保护作用
PI3K/Akt/FoxO3a/Bim signaling pathway mediated hydrogensulfide postconditioning-induced protection against H/R injury
摘要
Abstract
Aim To explore the role of PI3K/Akt/FoxO3a/Bim pathway in H9c2 cardiomyocytes cardioprotection of hydrogen sulfide(H2S) postconditioning against hypoxia/reoxygenation(H/R) injury.Methods H9c2 cells were subjected to 3h hypoxia followed by 6h reoxygenation.Cells were divided into 5 groups: control group(Control),hypoxia/Reoxygenation group(H/R), NaHS postconditioning group(H/R+NaHS), NaHS with inhibitor LY294002 group(H/R+NaHS+LY) and LY294002 group(H/R+LY).The survival percentage of H9c2 cells and the release of LDH were detected at pre-hypoxia and reoxygenation 6 h.The flow cytometry was used to determine cell apoptosis at the end of reoxygenation.The expressions of Akt,p-Akt,FoxO3a,p-FoxO3a,Bim were detected by Western blot.Immunofluorescence staining was used to determine the expression of FoxO3a.Results There were no differences between each group before hypoxia(P>0.05).At the end of reoxygenation, cell viability in H/R+NaHS group was significantly improved (P<0.05),and the release of LDH and cell apoptosis rates were significantly decreased(P<0.05).Meanwhile, the expression of p-Akt,p-FoxO3a and cytoplasm FoxO3a was significantly improved, and Bim was significantly decreased.But LY294002 abolished the myocardial protection effects of NaHS, and significantly decreased p-Akt,p-FoxO3a and cytoplasm FoxO3a level, and increased Bim level.Conclusion PI3K/Akt/FoxO3a/Bim signaling pathway mediates hydrogen sulfide postconditioning-induced protection against H/R injury.关键词
缺氧/复氧损伤/硫化氢/心肌保护/PI3K/Akt/FoxO3a/Bim/后处理Key words
hypoxia/reoxygenation injury/hydrogen sulfide/myocardial protection/PI3K/ Akt/FoxO3a/Bim/postconditioning分类
医药卫生引用本文复制引用
周波,钱坤,胡明珠,季永..PI3K/Akt/FoxO3a/Bim信号通路介导硫化氢后处理对缺氧H9c2心肌细胞的保护作用[J].中国药理学通报,2017,33(7):971-976,6.基金项目
无锡市医院管理中心医学科研面上项目(No YGZXM14017) （No YGZXM14017）
