消退素D1(resolvin D1)抑制小鼠激活型小胶质细胞对PC12细胞的损伤及机制

Resolvin D1 inhibits the injury of PC12 cells induced by activated microglia

目的探讨消退素D1(Rv D1)在小鼠活化BV-2小胶质细胞介导PC12神经元损伤中所起的作用及相关机制。方法BV-2细胞分为对照组、脂多糖(LPS)处理组、Rv D1联合LPS处理组和Rv D1组。各组BV-2细胞处理12 h、24 h,ELISA检测上清液中白细胞介素1β(IL-1β)、IL-6、肿瘤坏死因子α(TNF-α)的水平;收集以上各组细胞培养24 h的上清液培养PC12细胞24 h后,MTT法检测PC12细胞存活率,Western blot法检测各组BV-2细胞核因子κB p65(NF-κB p65)蛋白的水平。结果与对照组比较,LPS处理的PC12细胞存活率降低,BV-2细胞上清液中IL-1β、IL-6、TNF-α的水平均升高,NF-κB p65核转位增加;而与LPS处理组相比,Rv D1联合LPS处理组PC12细胞存活率升高,BV-2细胞上清液中IL-1β、IL-6、TNF-α的含量均降低,NF-κB p65核转位减少。结论 Rv D1可通过抑制NF-κB p65核转位,抑制LPS激活的BV-2细胞对PC12神经元的损伤。

Objective To investigate the effect of resolvin D1（Rv D1） on the injury of PC12 cells induced by activated BV-2 microglia and the related mechanisms.Methods BV-2 cells were divided into control group,lipopolysaccharide（LPS）-treated group, Rv D1-treated group and Rv D1 combined with LPS（Rv D1-LPS）-treated group.After BV-2 cells were incubated with the corresponding substances for 12 and 24 hours,the levels of interleukin-1β（IL-1β）,IL-6,tumor necrosis factor-α（TNF-α） in the supernatants were determined by ELISA.The culture supernatants of BV-2 cells were collected at 24 hours and added into PC12 cells for another 24-hour culture.Thereafter,the survival rate of PC12 cells was tested by MTT assay.The expression of NF-κB p65 protein in BV-2 cells was deteced by Western blotting.Results Compared with the control group,the survival rate of PC12 cells in the LPS group significantly decreased; the levels of IL-1β,IL-6 and TNF-α in the supernatant of BV-2 cells and the nuclear translocation of NF-κB p65 significantly increased in the LPS group.Compared with the LPS group,the survival rate of PC12 cells in Rv D1-LPS group was significantly elevated; the levels of IL-1,IL-6,TNF-α and the nuclear translocation of NF-κB p65 were significantly reduced in Rv D1-LPS group.Conclusion Rv D1 can inhibit the injury of PC12 cells induced by activated BV-2 microglia through inhibiting the nuclear translocation of NF-κB p65 and inflammatory factor levels in BV-2 cells.