【摘要】 目的阐明槐果碱（Sop）对低氧导致的大鼠心肌细胞系H9c2损伤的抑制作用及机制。方法将H9c2细胞暴露于1%O₂环境中,同时加入不同浓度（1、4和16 mmol/L）的Sop培养细胞48 h后,用MTT法测定细胞活力;用试剂盒分别检测LDH释放水平和MDA含量;用流式细胞仪检测细胞凋亡;用Western blot检测细胞中cleaved-caspase-3、p-PI3K和p-AKT的蛋白表达量。结果 Sop呈浓度依赖性减轻由低氧导致的H9c2细胞的细胞活力降低、LDH释放、MDA含量增高和细胞凋亡（P<0.05,P<0.01,P<0.001）。Sop呈浓度依赖性降低cleaved-caspase-3的表达（P<0.05,P<0.01,P<0.001）,同时也增加p-PI3K/PI3K和p-AKT/AKT的比率（P<0.05,P<0.01,P<0.001）。结论 Sop能减轻低氧导致的细胞损伤,对H9c2细胞发挥保护作用,且这一作用可能是通过增强PI3K/AKT信号活性来实现的。更多还原

【Abstract】 Objective To investigate the inhibitory effect and mechanism of sophoridine（Sop） on cell injury caused by hypoxia in rat myocardial cell line H9 c2. Methods H9 c2 cells were exposed to 1% O₂ and cultured with different concentrations（1, 4 and 16 mmol/L） of Sop for 48 h. Cell viability was measured by MTT assay. The release level of LDH and the content of MDA were determined by the kit methods. Cell apoptosis was detected by flow cytometry. The protein expression of cleaved-caspase-3, p-PI3 K and p-AKT was detected by Western blot. Results Sop alleviated the cell viability, LDH release, MDA content and hypoxia-induced apoptosis of H9 c2 cells in a concentration-dependent manner（P<0.05, P<0.01, P<0.001）. Sop decreased the cleaved-caspase-3 expression and increased the ratio of p-PI3 K/PI3 K and p-AKT/AKT in a concentration-dependent manner（P<0.05, P<0.01, P<0.001）. Conclusions Sop reduces hypoxia-induced cell injury and has a protective effect in vitro model of H9 c2 cells, the potential mechanism is enhancing the stimulation activity of PI3 K/AKT signal.更多还原