黑果枸杞对H2O2诱导的H9c2心肌细胞氧化应激损伤的保护作用研究

目的探讨黑果枸杞(Lrm)对H2O2诱导的H9c2心肌细胞氧化应激损伤的保护作用。方法建立H2O2诱导的H9c2心肌细胞氧化应激损伤模型,将H9c2心肌细胞分为空白组、模型组(H2O2400μmol/L)以及实验组(Lrm 1.00 g/L加H2O2400μmol/L)。实验组于H2O2刺激前加入Lrm预处理2 h,再加入H2O2干预6 h。观察各组细胞形态,MTT法测定细胞活力、TUNEL法测定细胞凋亡率、Western Blotting检测B淋巴细胞瘤-2(Bcl-2)、Bcl-2相关x基因(Bax)蛋白表达。结果与空白组相比,模型组细胞形态明显异常、细胞活力降低、凋亡率显著升高,差异有统计学意义(P0.05),抑制凋亡蛋白Bcl-2表达减少,同时促凋亡蛋白Bax表达增加;与模型组相比,实验组细胞形态得到明显改善、细胞活力升高、凋亡率显著降低(P0.05),抑制凋亡蛋白Bcl-2表达增加,同时促凋亡蛋白Bax表达减少,差异具有统计学意义(P0.05)。结论 Lrm能够有效改善H2O2干预后的H9c2心肌细胞形态,提高细胞活力及降低凋亡率,其减轻氧化应激损伤作用机制与上调Bcl-2蛋白表达和下调Bax蛋白表达有关。

Protective effects of Lycium ruthenicum Murr. on hydrogen peroxide-induced cellular oxidative stress injury in heart-derived H9c2 cells

Objective To explore the protective effects of Lycium ruthenicum Murr. (Lrm) on hydrogen peroxide (H2O2)-induced cellular oxidative stress injury in heart-derived H9c2 cells. Methods In this study,H2O2-induced injury in heart-derived H9c2 cells was established as cellular oxidative stress injury model. The H9c2 cells were divided into blank group,model group(H2O2400 μmol/L) and experimental group(Lrm 1.00 g/L +H2O2400 μmol/L). The Lrm group was pretreated with Lrm for 2 h before treated with H2O2for 6 h. Cellular morphology of all groups was observed. Cell viability(MTT assay),apoptosis rate (TUNEL assay),Bcl-2 and Bcl-2 relating x gene protein (Bax) expression were evaluated (Western Blotting). Results Compared with the blank group, abnormal cellular morphology, decreased cell activity,and increased apoptosis were observed in the model group(P<0.05). Anti-apoptotic Bcl-2 gene was less expressed while pro-apoptotic Bax protein level was increased. Compared with the model group, cellular morphology and activity was greatly improved in the experimental group with reduced apoptosis rate (P <0.05). The increased expression of Bcl-2 and reduction of Bax were also significantly different. Conclusion Our findings suggest that Lrm tended to improve the H9c2 myocardial cellular morphology, enhance cell activity and reduce apoptosis rate. Its mechanism of action in reducing oxidative stress injury may be related to the up-regulation of Bcl-2 as well as down-regulation of Bax protein expression.