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目的研究银杏内酯B对抑制雷帕霉素诱导血管内皮细胞损伤的保护及可能的机制。方法通过5×10-7mol/L雷帕霉素损伤血管内皮细胞模型,考察银杏内酯B对雷帕霉素损伤后血管内皮细胞生长及粘附作用的影响,并采用Westernblot方法探索其可能的机制。结果银杏内酯B在40μg/ml的浓度能够抑制雷帕霉素对血管内皮细胞的损伤,可能是通过下调p38MAPK信号通路途径抑制雷帕霉素对血管内皮细胞的损伤。结论银杏内酯B能通过调控p38MAPK的途径有效抑制雷帕霉素对血管内皮细胞的损伤。
Objective To study the protective effect of ginkgolide B on rat rapamycin-induced vascular endothelial cell injury and its possible mechanism. Methods The effects of ginkgolide B on the growth and adhesion of vascular endothelial cells after rapamycin injury were investigated by 5 × 10-7mol / L rapamycin-induced injury of vascular endothelial cells. The potential of this method was explored by Western blot mechanism. Results Ginkgolide B inhibited the injury of vascular endothelial cells by rapamycin at a concentration of 40μg / ml, which may be due to the downregulation of p38MAPK signaling pathway to inhibit the damage of rapamycin to vascular endothelial cells. Conclusion Ginkgolide B can effectively inhibit the injury of vascular endothelial cells by rapamycin through regulating the pathway of p38MAPK.