Xi Ming-Ming, Liu Jing, Xie Liang, Gong Jian-Bin
Department of Cardiology, Taizhou People's Hospital, Taizhou 225300, China.E-mail:
Nan Fang Yi Ke Da Xue Xue Bao. 2016 Aug 20;36(9):1198-1203.
To investigated the effects of bisoprolol pretreatment on hypoxia/reoxygenation (H/R)-induced injury in H9c2 cardiomyocytes.
Cultured H9c2 cells were exposed to hypoxia for 6 h followed by reoxygenation for 2 h with or without pretreatments with bisoprolol or bisoprolol + LY294002. The cell survival was measured by MTT assay, and the cell apoptosis and levels of radical oxygen species (ROS) were evaluated with flow cytometry. The protein levels of phosphyorylated AKT and phosphorylated GSK3β in the cells were determined by Western blotting.
Compared with the normal control cells, the cells exposed to H/R injury showed significantly decreased cell survival and increased cell apoptosis and ROS production; pretreatment of the cells with bisoprolol significantly decreased the cell apoptotic rates and ROS production and obviously enhanced the cell survival and protein levels of p-AKT and p-GSK3β in the exposed cells. The protective effect of bsioprolol against H/R-induced cell injury was significantly attenuated by LY294002.
Bisoprolol can protect H9c2 cells against H/R-induced injury and oxidative stress by activating PI3K/AKT/Gsk-3β pathway to increase the phosphorylation of AKT and GSK3β and reduce ROS production.
研究比索洛尔预处理对H9c2心肌细胞缺氧/复氧（H/R）诱导损伤的影响。
将培养的H9c2细胞暴露于缺氧环境6小时，然后在有或无比索洛尔或比索洛尔+LY294002预处理的情况下进行2小时复氧。通过MTT法测定细胞存活率，并用流式细胞术评估细胞凋亡和活性氧（ROS）水平。通过蛋白质印迹法测定细胞中磷酸化AKT和磷酸化GSK3β的蛋白质水平。
与正常对照细胞相比，暴露于H/R损伤的细胞显示细胞存活率显著降低，细胞凋亡和ROS产生增加；用比索洛尔预处理细胞可显著降低细胞凋亡率和ROS产生，并明显提高暴露细胞的存活率以及p-AKT和p-GSK3β的蛋白质水平。LY294002显著减弱了比索洛尔对H/R诱导的细胞损伤的保护作用。
比索洛尔可通过激活PI3K/AKT/Gsk-3β通路，增加AKT和GSK3β的磷酸化并减少ROS产生，从而保护H9c2细胞免受H/R诱导的损伤和氧化应激。
