PI3K/Akt信号通路在瓜蒌皮保护心肌细胞缺氧/复氧损伤中的作用

目的研究PI3K/Akt信号通路在瓜蒌皮保护心肌细胞缺氧/复氧损伤中的作用。方法以2.5 mmol/L Na2S2O4诱导心肌细胞建立缺氧/复氧损伤模型,实验分为正常组、模型组、瓜蒌皮提取物组及抑制剂组。应用MTT法检测细胞活力;流式细胞术观察细胞凋亡情况;Western Blot测定Akt、p-Akt(Ser 473)、Bax、Bcl-2的蛋白表达水平。结果与模型组相比,瓜蒌皮提取物预处理24 h后能改善心肌细胞形态,明显提高心肌细胞活力。瓜蒌皮提取物能促进Akt、p-Akt(Ser 473)及抗凋亡蛋白Bcl-2的表达,抑制促凋亡蛋白Bax的表达,减少心肌细胞凋亡。PI3K抑制剂LY294002与瓜蒌皮提取物联合处理后,逆转了瓜蒌皮提取物对心肌细胞的上述作用,导致细胞凋亡率上升。结论瓜蒌皮提取物可能通过激活PI3K/Akt信号通路改善缺氧/复氧损伤诱导的心肌细胞凋亡。

Trichosanthis Pericarpium Aqueous Extract Alleviates Hypoxia/Reoxygenation Injury in H9c2 Cardiomyocytes by Regulating PI3K/Akt

Objective To investigate the effects of Gualoupi(Trichosanthis Pericarpium) extract(TPE) protecting H9 c2 cells from hypoxia/reoxygenation injury through activation of the PI3 K/Akt signaling pathway. Methods A treatment of 2.5 mmol/L Na2S2O4 for 30 min and replacing the normal media for 4 h was applied to induce H9 c2 cardiomyocytes H/R injury in the experiments. The cultured H9 c2 cardiomyocytes were randomly divided into normal group, H/R group(model group),TPE group and inhibiting group. The cell viability was measured by MTT assay. The apoptotic rate was detected by Annexin V-FITC/PI staining. Western blotting was used to detect the expressions of Akt, p-Akt, Bcl-2 and Bax. Results Compared with the H/R group, the pretreatment of TPE remarkably enhanced the cell viability 24 h after pretreatment. TPE can up-regulate the protein expressions of Akt, p-Akt and Bcl-2, and down-regulate the level of Bax. LY294002,a specific chemical inhibitor of PI3 K, was used. Obviously,the cardioprotection effect of TPE was blocked by LY294002 co-treatment and the cell apoptosis was correspondingly reversed. Conclusion TPE can protect H9 c2 cardiomyocytes from H/R injury, at least in part via activating the PI3 K/Akt signaling pathway.