摘要
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 The effect of ginkgolide B on the inhibition of rapamycin induced the injury of endothelial cellsand the possible mechanism. Methods We use 5 × 10-7mol / L rapamycin,vascular endothelial cell injury model,effects of ginkgolide B on rapamycin after injury of vascular endothelial cell growth and adhesion,and using the Westernblot method to explore the possible mechanism of. Results Ginkgolide B can inhibit the effect of rapamycin on the injury of vascular endothelial cells in aconcentration of 40 ug / ml,possibly through down-regulation of Ginkgolide B can inhibit the effect of rapamycin on the injury of vascular endothelial cells in aconcentration of 40 ug / ml,possibly through down-regulation of Conclusion Ginkgolide B can through the way of regulating p38 MAPK effectively inhibits the effect of rapamycin on vascular endothelial cell injury.
出处
《时珍国医国药》
CAS
CSCD
北大核心
2016年第9期2049-2051,共3页
Lishizhen Medicine and Materia Medica Research
基金
国家自然科学基金(No.81303145)
