姜黄素调控KLF2表达对BV2细胞OGD模型中的作用及机制

Effect and Mechanism of Curcumin Regulating KLF2 Expression on Oxygen-Glucose Deprivation(OGD)Model of BV2 Cells

目的:研究姜黄素对氧糖剥夺(OGD)模型损伤神经元的保护作用并探讨其机制。方法:采用BV2细胞在OGD环境中培养2h模拟神经元缺血缺氧损伤,MTT法检测BV2小胶质细胞活力,Western blot法检测KLF2、p-NF-κB、NF-κB蛋白的表达水平;ELISA法检测炎症因子TNF-α、IL-1β的含量。结果:与Control组相比,OGD组BV2细胞活力显著降低,KLF2蛋白表达下降,p-NF-κB蛋白表达增高,炎症因子TNF-α、IL-1β水平增高(P<0.05);10μmol/L的姜黄素可显著增加OGD诱导的BV2细胞活力,上调KLF2蛋白表达,下调p-NF-κB的表达,降低炎症因子的水平(P<0.05)。而KLF2-si RNA显著逆转姜黄素对OGD诱导的BV2细胞上述保护作用(P<0.05)。结论:姜黄素上调KLF2的表达并降低促炎细胞因子TNF-α、IL-1β的水平,其机制可能通过抑制NF-κB信号通路来实现对神经元缺血缺氧损伤的神经保护作用。

Objective:To study the protective effect of curcumin on neurons damaged by Oxygen-Glucose Deprivation(OGD)model and explore its mechanism.Methods:BV2 microglia were exposed to OGD for 2 hours to simulate neuronal ischemia and hypoxia injury.The viability of BV2 microglia was detected by Methylthiazolyldiphenyl-tetrazolium bromide(MTT)colorimetric method.The expression levels of KLF2,p-NF-κB and NF-κB proteins were detected by Western blot.The levels of inflammatory cytokines TNF-αand IL-1βwere detected by ELISA.Results:Compared with Control group,the activity of BV2 cells in OGD group was significantly decreased,the expression of KLF2 protein was decreased,the expression of p-NF-κB protein was increased,and the levels of inflammatory factors TNF-αand IL-1βwere increased(P<0.05).Curcumin at 10μmol/L significantly increased the activity of BV2 cells induced by OGD,up-regulated the expression of KLF2 protein,down-regulated the expression of p-NF-κB,and decreased the level of inflammatory factors(P<0.05).However,KLF2-si RNA significantly reversed the protective effect of curcumin on OGD-induced BV2 cells(P<0.05).Conclusion:Curcumin up-regulates the expression of KLF2 and decreases the levels of TNF-αand IL-1β.The mechanism of curcumin may inhibit NF-κB signaling pathway to achieve neuroprotective effect on neuronal hypoxia-ischemia injury.