桃叶珊瑚苷通过调节小胶质细胞M1/M2极化抑制神经炎症

Aucubin inhibits neuroinflammation by regulating the M1/M2 polarization of microglia

目的:探究桃叶珊瑚苷(aucubin)对脂多糖(LPS)诱导建立的体外神经炎症模型的影响。方法:用LPS诱导N9细胞激活建立体外神经炎症模型,加入桃叶珊瑚苷处理细胞24 h,对细胞上清一氧化氮(NO)含量和细胞活力进行检测,显微镜拍摄细胞形态,免疫荧光法检测小胶质细胞特异标志物Iba-1水平,Flowsight检测CD11b水平和CD86/CD206比值,并用试剂盒检测IL-4,IL-10,TGF-β,IL-1β,IL-6,TNF-α水平。结果:与模型对照组比较,桃叶珊瑚苷组可有效改善细胞形态,降低细胞上清NO含量,降低细胞标志物CD11b水平和CD86/CD206比值,并调节炎症因子的释放。结论:桃叶珊瑚苷可能是通过调控炎症因子的释放,促进小胶质细胞由M1型向M2型转化,从而抑制N9小胶质细胞的激活,最终抑制LPS诱导的神经炎症。

Objective:To investigate the anti-neuroinflammatory effect of Aucubin extracted from Rehmannia glutinosa in lipopolysaccharide(LPS)-induced neuroinflammation model in vitro.Methods:N9 cells were activated by 10μg mL-I LPS to establish an in vitro neuroinflammatory model.After treatment with Aucubin for 24 h,NO content was detected by Griess method,cell viability was detected by MTT method,cell morphology was photographed by microscopy,the level of Iba-1(a specific marker of microglia)was detected by immunofluorescence,CD1lb level and CD86/CD206 ratio were determined by flowsight assay,and the levels of IL-6,IL-1β,IL-4 and IL-10 were detected by kits.Results:Compared with the model group,the aucubin group effectively improved cell morphology,reduced cell supernatant NO level,decreased cell marker CD11b level and CD86/CD206 value,and regulated the release of inflammatory factors.Conclusions:Aucubin inhibited the activation of microglia to M1 phenotype and promoted the transformation of M2 phenotype.It also regulated the release of inflammatory factors thus inhibited the activation of N9 microglia and finally suppressed LPS-induced neuroinflammation.