牡荆素对脂多糖诱导牙髓干细胞表达炎症因子的影响  

Influence of vitexin on the expression of inflammatory cytokines in dental pulp stem cells induced by lipopolysaccharide

作　　者：牛晨光 李佳洋 於丽明 陈栋[1] 韦晓玲 NIU Chen-guang;LI Jia-yang;YU Li-ming;CHEN Dong;WEI Xiao-ling(Oral Biomedical Engineering Laboratory,Shanghai Stomatological Hospital,Fudan University.Shanghai 200001,China)

机构地区：[1]上海市口腔病防治院,复旦大学附属口腔医院口腔生物医学工程实验室,上海200001

出　　处：《上海口腔医学》2020年第5期462-465,共4页Shanghai Journal of Stomatology

基　　金：上海市卫生和计划生育委员会科研课题(201740051)。

摘　　要：目的:探讨牡荆素(vitexin,VTX)对脂多糖(lipopolysaccharide,LPS)诱导的人牙髓干细胞(human dental stem pulp cells,hDPSCs)表达炎症因子的影响,并初步探讨其相关作用机制。方法:分离、培养hDPSCs,以CCK-8法检测VTX对hDPSCs增殖的影响,检测VTX毒性浓度范围。铺种hDPSCs,分为4组,空白组以不含LPS和VTX的无血清DMEM,LPS组仅加入含LPS终浓度为2μg/mL的无血清DMEM培养,VTX处理组1(V1组)加入2μg/mL LPS+25μmol/L VTX,VTX处理组2(V2组)加入2μg/mL LPS+50μmol/L VTX。培养48 h,实时荧光定量PCR检测各组细胞中IL-1β、IL-6及IL-8基因转录,蛋白质免疫印迹检测hDPSCs内MPAK信号通路及COX-2等蛋白的变化。采用SPSS 16.0软件包对数据进行统计学分析。结果:VTX在200μmol/L范围内时细胞活力不受影响(P>0.05);VTX抑制LPS刺激hDPSCs转录IL-1β、IL-6及IL-8,抑制效果与VTX的浓度呈正相关;VTX可显著抑制LPS激活p38及ERK信号通路。结论:VTX可能通过抑制p38及ERK信号通路的激活,降低LPS诱导的hDPSCs转录IL-1β、IL-6及IL-8。PURPOSE:To investigate the effect of vitexin(VTX)on the expression of inflammatory cytokines in human dental pulp stem cells(hDPSCs)induced by lipopolysaccharide(LPS),and to explore the underlying mechanism.METHODS:hDPSCs were isolated and cultured,and CCK-8 method was used to detect the effect of VTX on proliferation of hDPSCs.hDPSCs were randomly divided into 4 groups:blank group(without LPS and VTX),LPS group(2μg/mL LPS),2μg/mL LPS+25μmol/L VTX,2μg/mL LPS+50μmol/L VTX.The cells of all groups were cultured for 48 h.The gene levels of IL-1β,IL-6 and IL-8 in hDPSCs were detected by real time qPCR(RT-qPCR).The change of COX-2 and MAPKs signaling pathways were detected by Western blot.SPSS 16.0 software package was used for statistical analysis.RESULTS:When the VTX concentration was less than 200μmol/L,the cell viability was not affected(P>0.05).VTX at 25 and 50μmol/L significantly reduced LPS-induced expression of IL-1β,IL-6 and IL-8 at gene levels and COX-2 at protein level(P<0.05).CONCLUSIONS:VTX significantly inhibited the activation of ERK and p38 signaling pathway.VTX can reduce LPS-induced inflammatory cytokine expression in hDPSCs via restraining the activation of ERK and p38 signaling pathway.

关 键 词：牡荆素 人牙髓干细胞 炎症因子 MAPK 

分 类 号：R781.3[医药卫生—口腔医学]