N-n-butyl haloperidol iodide protectsH9c2 cardiac myocytes against hypoxia/reoxygenationinjury through mitochondria-dependent apoptotic pathway

VernacularTitle:碘化N-正丁基氟哌啶醇通过抑制线粒体凋亡通路抗H9c2心肌细胞缺氧/复氧损伤
Author: Bin WANG ; Danmei HUANG ; Yuanhang WANG ; Qiaoling ZHOU ; Hong LIN ; Yanmei ZHANG ; Ganggang SHI ; Fuchun ZHENG
Keywords: N-n-butyl haloperidol iodide; hypoxia/reoxygenation; H9c2 cardiac myocytes; apoptosis; mitochondria; cytochrome C
From: Chinese Pharmacological Bulletin 2017;33(6):819-823
CountryChina
Language:Chinese
Abstract: Aim To investigate the effect of N-n-butyl haloperidol iodide(F2) on mitochondria-dependent apoptotic pathway of H9c2 cardiac myocytes during hypoxia/reoxygenation(H/R) injury.Methods The H/R models of H9c2 cardiac myocytes were established.The H9c2 cardiac myocytes were randomly divided into five groups: control group(C group), hypoxia/reoxygenation group(H/R group), F2 low concentration group(L), F2 medium concentration group(M), F2 high concentration group(H).Apoptotic rate was evaluated by flow cytometry(FCM).The levels of Cyto C, Bcl-2, Bax were observed by Western blot.Caspase-3 activity was measured with colorimetry.Results Compared with H/R group, F2 low, medium and high concentrations group could significantly decrease apoptosis rate and increase the ratio of Bcl-2 to Bax proteins and inhibit the release of Cyto C into the cytosolic fraction, and decrease caspase-3 activity.Conclusion F2 can protect H9c2 cardiac myocytes against H/R-induced injury through interfering in mitochondria-dependent pathway.