梓醇激活Nrf2/HO-1信号通路对高糖诱导EA.hy926细胞损伤的影响

Catalpol reduces the endothelial cells injury induced by high glucose through activating Nrf2 signaling pathway

目的观察梓醇对高糖诱导EA.hy926细胞损伤的影响,并以Nrf2/HO-1信号通路为靶点探讨其可能的作用机制。方法将常规培养的EA.hy926细胞随机分为对照组(A组)、梓醇组(B组,0.5mmol/L)、高糖组(C组,100mg/L)、梓醇高剂量保护组(D组,0.5mmol/L)、梓醇低剂量保护组(E组,0.05mmol/L)。MTT法检测细胞活性;Hoechst细胞核染色检测细胞凋亡比率;ELISA法检测肿瘤坏死因子-α(TNF-α)、白介素-6(IL-6)的含量;Western-blot检测核因子E2相关因子2(Nrf2)及血红素加氧酶1(HO-1)的表达。结果梓醇保护组细胞损伤明显减轻,TNF-α,IL-6明显减少,Nrf2和HO-1表达显著升高,且呈剂量依赖性(P<0.05)。结论梓醇能够有效减轻高糖诱导EA.hy926细胞损伤,保护EA.hy926细胞,其机制可能与其激活Nrf2/HO-1信号通路抑制炎症反应有关。

Objective The aim of the present study was to observe the effect of catalpol on the damage of high glucose-induced in EA.hy926 cells and to explore the possible mechanism of Nrf2/HO-1 signaling pathway.Methods EA.hy926 cells were cultured and randomly divided into control group(A group),catalpol group(B group, 0.5 mmol/L),high glucose group(C group, 100 mg/L),catalpol protection group high-dose(D group, 0.5 mmol/L),low-dose group(E group, 0.05 mmol/L).Viability and apoptosis ratio of EA.hy926 cells were determinted by MTT and Hoechst staining respectively.The inflammatory cytokines TNF-α,IL-6 were detected by ELISA.Expression of Nrf2 and HO-1 protein were detected by Western-blot.Results EA.hy926 cells were injured very slightly in catalpol protection group, the contents of TNF-α and IL-6 were decreade significantly, the expression of Nrf2 and HO-1 increased significantly in a dose-dependent manner(P<0.05).Conclusion Catalpol can effectively reduce the damage of high glucose-induced in EA.hy926 cells, which may be related to activation of Nrf2/HO-1 signaling pathway and inhibition inflammatory response.