【摘要】 目的:探讨红花黄色素(SY)对小鼠源永生细胞系小胶质细胞(BV2细胞)进行糖氧剥夺/复氧(OGD/R)处理后炎性反应的影响及其抗炎作用的机制。方法:BV2细胞进行常规培养和传代,细胞长到90%左右后建立OGD/R模型。实验分为正常组、OGD/R组、OGD/R联合SY干预(OGD/R+SY)组。MTT法检测BV2细胞的活性以评价SY的细胞毒性作用,免疫印迹法检测炎性信号通路TLR4、p-NF-κB(p65)蛋白表达情况,ELISA检测BV2细胞白细胞介素-6(IL-6)、白细胞介素-1β(IL-1β)、肿瘤坏死因子-α(TNF-α)的炎性因子释放。结果:BV2细胞经OGD/R处理后,TLR4、p-NF-κB(p65)蛋白表达升高,SY可以抑制其升高并下调IL-6、IL-1β、TNF-α炎性因子的分泌。结论:OGD/R可能通过激活BV2细胞TLR4-NF-κB信号通路,引发炎性反应;SY可以通过抑制TLR4-NF-κB信号通路而发挥抗炎作用。更多还原

【Abstract】 Objective: To investigate the anti-inflammatory effect and related mechanism of safflower yellow(SY) on microglia BV2 with oxygen glucose deprivation/reoxygenation(OGD/R). Methods: BV2 cells were routinely cultured and passed, and OGD/R cell model was established after the cells grow up to about 90%. The study included three groups: normal group, OGD/R group and OGD/R plus SY(OGD/R+SY) group. Toxic effect of SY on BV2 cells was detected by MTT assay, expressions of TLR4 and NF-κB(p65) protein were examined by western blot, and production levels of IL-6, IL-1β and TNF-αwere examined by ELISA. Results: After treating with OGD/R, expressions of TLR4 and p-NF-κB(p65) protein in BV2 cells were increased. SY could inhibit the increasing of TLR4 and p-NF-κB(p65) expression, and down-regulate the secretion of IL-6, IL-1β and TNF-α in BV2 microglia. Conclusion: OGD/R could cause imflammatory reaction by activating TLR4/NF-κB signaling pathway in BV2 microglia. SY could reverse OGD/R-induced inflammatory response in BV2 microglia by inhibiting TLR4/NF-κB signaling pathway.更多还原