三七总皂苷通过p38 MAPK通路抑制内毒素诱导的小胶质细胞活化  

Panax notoginseng saponins inhibit LPS-induced microglia activation through p38 MAPK pathway

作　　者：段兆达 王健翔 杨力 徐冬垚 祁志 吴春云 贾文姬[2] DUAN Zhaoda;WANG Jianxiang;YANG Li;XU Dongyao;QI Zhi;WU Chunyun;JIA Wenji(Department of Human Anatomy,Histology and Embryology,School of Basic Medical,Kunming 650500;The Second Affiliated Hospital,Kunming Medical University,Kunming 650000,China;Affiliated Galmette Hospital,Kunming Medical University,Kunming 650000,China)

机构地区：[1]昆明医科大学基础医学院人体解剖与组织胚胎学系,昆明650500 [2]昆明医科大学第二附属医院,昆明650000 [3]昆明医科大学附属甘美医院,昆明650000

出　　处：《神经解剖学杂志》2024年第2期196-202,共7页Chinese Journal of Neuroanatomy

基　　金：国家自然科学基金(81960223);云南省科技厅联合专项(202001AY070001-217)。

摘　　要：目的:探讨三七总皂苷(PNS)通过p38丝裂原活化蛋白激酶(p38 MAPK)通路对脂多糖(LPS)诱导活化的BV2小胶质细胞中肿瘤坏死因子-α(TNF-α)表达的影响。方法:将BV2小胶质细胞分为空白对照组(Control)、LPS激活组和LPS+三七总皂苷干预组(LPS+PNS)。CCK-8法检测BV2小胶质细胞的活力,确定最适合的药物干预浓度。利用Western Blot和免疫荧光检测BV2小胶质细胞中p38 MAPK和TNF-α的表达及p38 MAPK磷酸化水平(p-p38 MAPK)变化。结果:与空白对照组相比,PNS对BV2小胶质细胞的细胞活力无显著差异,最终选定100 mg/L作为药物干预浓度。Western Blot、免疫荧光结果提示,LPS激活后,BV2小胶质细胞中TNF-α的表达显著升高,p38 MAPK磷酸化水平增加(P<0.05);PNS干预后,与LPS激活组相比,TNF-α表达显著下降,p38 MAPK磷酸化水平降低(P<0.05)。使用p38 MAPK通路抑制剂(SB203580)作用后,PNS联合SB203580组(LPS+PNS+SB203580)中,TNF-α表达及p38 MAPK磷酸化水平变化与LPS+PNS组相比无显著差异(P>0.05)。此外,p38 MAPK在各组的变化无显著性差异(P>0.05)。结论:PNS可能通过p38 MAPK通路抑制活化的BV2小胶质细胞分泌的炎性因子TNF-α的表达。Objective:To investigate the effect of panax notoginseng saponins(PNS)on the expression of tumor necrosis factor-α(TNF-α)in lipopolysaccharide(LPS)-induced activated BV2 microglia through p38 mitogen-activated protein kinase(p38 MAPK)pathway.Methods:BV2 microglia were divided into control group,LPS activated group and LPS+panax notoginseng saponins intervention group(LPS+PNS).The CCK-8 method was used to detect the viability of BV2 microglia and determine the optimal drug intervention concentration.Western Blot and immunofluorescence were used to detect the expression of p38 MAPK and TNF-αand the phosphorylation level of p38 MAPK(p-p38 MAPK)in BV2 microglia.Results:Compared with the blank control group,there was no significant difference in the cell viability of BV2 microglia,and finally 100 mg/L was selected as the drug intervention concentration.Western Blot and immunofluorescence results indicated that after LPS activation,the expression of TNF-αand the phosphorylation level of p38 MAPK in BV2 microglia were significantly increased(P<0.05).After PNS intervention,compared with LPS-activated group,the expression of TNF-αand the phosphorylation level of p38 MAPK were significantly decreased(P<0.05).After treatment with p38 MAPK pathway inhibitor(SB203580),there was no significant difference in the expression levels of p-p38 MAPK and TNF-αin PNS combined with SB203580 group(LPS+PNS+I)compared with LPS+PNS group(P>0.05).In addition,the changes of p38 MAPK in each group were not statistically significant(P>0.05).Conclusion:PNS may inhibit the expression of inflammatory factor TNF-αsecreted by activated BV2 microglia through p38 MAPK pathway.

关 键 词：三七总皂苷(PNS) p38丝裂原活化蛋白激酶(p38 MAPK) 脂多糖(LPS) 肿瘤坏死因子-α(TNF-α) BV2小胶质细胞 

分 类 号：R285.5[医药卫生—中药学]