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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 role of Rv D1 in the activation of BV12 microglia-mediated PC12 neuron injury in mice and its related mechanisms. Methods BV-2 cells were divided into control group, lipopolysaccharide (LPS) treatment group, Rv D1 combined with LPS treatment group and Rv D1 group. The levels of IL-1β, IL-6 and TNF-α in supernatant of BV-2 cells in each group were measured after 12 h, 24 h. After cultured for 24 h, the PC12 cells were cultured for 24 h. The survival rate of PC12 cells was detected by MTT assay. The level of NF-κB p65 protein in BV-2 cells was detected by Western blot. Results Compared with the control group, the survival rate of PC12 cells treated with LPS decreased and the levels of IL-1β, IL-6 and TNF-α in BV-2 cells increased and the nuclear translocation of NF-κB p65 increased Compared with LPS treatment group, the survival rate of PC12 cells increased in the combination of Rv D1 and LPS treatment, and the levels of IL-1β, IL-6 and TNF-α in BV-2 cells supernatant decreased, and the nuclear translocation of NF-κB p65 Bit reduction. Conclusion Rv D1 can inhibit the damage of PC12 neurons by LPS-activated BV-2 cells by inhibiting nuclear translocation of NF-κB p65.