人参皂苷Rg1 对阿霉素引起的血管内皮细胞 损伤的作用及机制研究

Ginsenoside Rg1 protects against endothelial cell injury induced by doxorubicin through antioxidation and anti-apoptosis

摘要:

目的 探讨人参皂苷Rg1 对阿霉素损伤后血管内皮细胞的作用及其机制。方法 该研究分为 正常组、阿霉素组（0.5μg/ml）、阿霉素+Rg1 组（0.5μg/ml 阿霉素+200μg/ml Rg1）。通过MTT 法、划 痕及小管形成实验检测人参皂苷Rg1 对阿霉素损伤后血管内皮细胞增殖、迁移及小管形成的影响。通过 Hochst33342 染色和流式细胞术检测人参皂苷Rg1 对阿霉素损伤后血管内皮细胞凋亡的影响。采用Western blotting 检测人参皂苷Rg1 对阿霉素损伤后血管内皮细胞Bcl-2、p-Akt、p-ERK 及p-eNOS 蛋白表达的影 响。结果 与正常组比较，阿霉素组细胞活性降低（P <0.05）；与阿霉素组比较，阿霉素+Rg1 组能提高血管 内皮细胞的细胞活性（P <0.05）。与阿霉素组比较，阿霉素+Rg1 组能够改善血管内皮细胞的迁移及小管形 成状态（P <0.05）。与阿霉素组比较，阿霉素+Rg1 组减少阿霉素引起的细胞凋亡（P <0.05）。与阿霉素组比较， 阿霉素+Rg1 组阿霉素损伤后血管内皮细胞NO 升高（P <0.05），ROS 减少（P <0.05）。阿霉素组Bcl-2、 p-ERK、p-Akt 及p-eNOS 蛋白相对表达量较正常组低（P <0.05），阿霉素+Rg1 组较阿霉素组高（P <0.05）。 结论 人参皂苷Rg1 可减轻阿霉素引起的血管内皮细胞损伤，从而为人参皂苷Rg1 治疗阿霉素引起的心脏损 伤提供新的靶点。

Abstract:

Objective To investigate the protective effect of ginsenoside Rg1 on vascular endothelial cells injured by doxorubicin and to explore its mechanism. Methods The study consists of normal group, doxorubicin group (0.5 μg/ml) and doxorubicin + Rg1 group (0.5 μg/ml doxorubicin + 200 μg/ml Rg1). The effects of ginsenoside Rg1 on proliferation, migration and tube formation of vascular endothelial cells after injury with doxorubicin were respectively detected by MTT, scratch assay and tubule formation assay. The apoptosis of vascular endothelial cells induced by doxorubicin was detected by Hochst33342 staining and flowcytometry. The effects of ginsenoside Rg1 on the expression of Bcl-2, p-Akt, p-ERK and p-eNOS in vascular endothelial cells injured by doxorubicin were determined by immunoblotting. Results After doxorubicin injury, ginsenoside Rg1 promoted proliferation, migration and tube formation of vascular endothelial cells (P < 0.05), and decreased apoptosis of vascular endothelial cells (P < 0.05). Besides, compared to those of the doxorubicin group, NO was increased while ROS was reduced in the injured vascular endothelial cells of doxorubicin+Rg1 group (P < 0.05). Western blot results showed that ginsenoside Rg1 increased the expression of Bcl-2, p-Akt, p-ERK and p-eNOS in vascular endothelial cells injured by doxorubicin (P < 0.05). Conclusions Ginsenoside Rg1 attenuates vascular endothelial cell injury induced by doxorubicin, which provides a new target for the treatment of cardiac damage caused by doxorubicin.