车前草苷通过抑制NF-κB/IL-6信号通路减弱LPS诱导的人牙龈成纤维细胞的炎症反应

Plantamajoside Attenuates LPS-Induced Inflammatory Response of Human Gingival Fibroblasts by Inhibiting the NF-κB/IL-6 Signaling Pathway

目的:探究车前草苷(PMS)通过抑制核因子-κB(NF-κB)/白细胞介素-6(IL-6)信号通路对脂多糖(LPS)诱导的人牙龈成纤维细胞的炎症反应的影响。方法:将培养的人牙龈成纤维细胞(HGnF)随机分为:对照组、模型组(10mg/L LPS)、PMS低、高剂量组(50、100μg/mL PMS+10mg/L LPS)、激活剂组(10μM BAY11-7085+10mg/L LPS)、PMS高剂量+激活剂组(10μM BAY11-7085+100μg/mL+10mg/L LPS)。CCK-8法检测HGnF细胞活力,ELISA法检测HGnF细胞上清液中白细胞介素1β(IL-1β)、白细胞介素6(IL-6)、白细胞介素18(IL-18)含量,Western blot法检测诱导型一氧化氮合酶(iNOS)、IL-1β及NF-κB/IL-6信号通道相关蛋白表达水平。结果:低、高剂量PMS可升高LPS诱导的HGnF细胞活力,降低上清液IL-1β、IL-6、IL-18含量、细胞IL-1β、iNOS及p-NF-κB/NF-κB、IL-6表达水平(P<0.05);激活剂BAY11-7085逆转了高剂量PMS对LPS诱导的HGnF细胞的上述指标的作用(P<0.05)。结论:PMS可能通过抑制NF-κB/IL-6信号通路改善由LPS诱导HGnF细胞的炎症。

Objective:To explore the effect of plantamajoside(PMS)on the inflammatory response of human gingival fibroblasts induced by lipopolysaccharide(LPS)by inhibiting nuclear factor-κB(NF-κB)/interleukin-6(IL-6)signaling pathway.Methods:The cultured human gingival fibroblasts(HGnF)were randomly divided into control group,model group(10mg/L LPS),PMS low and high-dose groups(50,100μg/mL PMS+10mg/L LPS),activator group(10μM BAY11-7085+10mg/L LPS),and PMS high-dose+activator group(10μM BAY11-7085+100μg/mL+10mg/L LPS).CCK-8 method was used to detect HGnF cell viability,ELISA method was used to detect the contents of interleukin 1β(IL-1β),interleukin 6(IL-6),and interleukin 18(IL-18)in the supernatant of HGnF cells.Western blot method was used to detect the expression levels of inducible nitric oxide synthase(iNOS),IL-1βand NF-κB/IL-6 signaling pathway-related proteins.Results:Low and high-doses PMS could increase the cell viability of HGnF induced by LPS,decrease the contents of IL-1β,IL-6,IL-18 in supernatant,and the expression levels of IL-1β,iNOS,p-NF-κB/NF-κB,and IL-6 in cells(P<0.05).The activator BAY11-7085 reversed the effects of high-dose PMS on the above indicators in LPS-induced HGnF cells(P<0.05).Conclusion:PMS may improve the inflammation of HGnF cells induced by LPS by inhibiting the NF-κB/IL-6 signaling pathway.