SOCS6通过JAK2/STAT3信号通路对人牙周膜成纤维细胞炎症及凋亡的影响  

Effects of SOCS6 on Inflammation and Apoptosis of Human Periodontal Ligament Fibroblasts through JAK2/STAT3 Signaling Pathway

作　　者：邱枫 杜宇 罗惠冰 刘星 QIU Feng;DU Yu;LUO Huibing;LIU Xing(Department of General Dentistry,Foshan Chancheng People's Hospital,Foshan 528000,China;School of Medicine,Jinggangshan University,Ji'an 343009,China)

机构地区：[1]佛山市禅城区人民医院口腔综合科,广东佛山528000 [2]井冈山大学医学部,江西吉安343009

出　　处：《口腔医学研究》2023年第9期815-820,共6页Journal of Oral Science Research

基　　金：佛山市科技创新项目(编号:2220001005553)。

摘　　要：目的:探究SOCS6通过JAK2/STAT3信号通路对人牙周膜成纤维细胞(hPDLFs)炎症及凋亡的影响。方法:取对数生长期的hPDLFs,分组如下:对照组、0.1 mg/L LPS组、1 mg/L LPS组、5 mg/L LPS组,qRT-PCR观察LPS对hPDLFs中SOCS6 mRNA表达的影响,Western blot观察LPS对hPDLFs中SOCS6蛋白表达的影响,CCK-8法观察LPS对hPDLFs细胞活力的影响,ELISA法观察LPS对hPDLFs细胞炎症因子TNF-α、IL-1β的含量的影响。慢病毒滴度检测、靶细胞感染预实验及细胞转染,并且qRT-PCR检测细胞SOCS6 mRNA表达。取对数生长期的hPDLFs,过表达转染SOCS6后,LPS诱导hPDLFs炎症细胞模型,用JAK2信号激活剂香豆霉素A1(CA1)处理过夜,分组如下:LPS组(5 mg/L LPS)、LPS+oe-NC组、LPS+oe-SOCS6组、LPS+oe-SOCS6+CA1组,CCK-8法检测各组细胞活力,流式细胞术检测各组细胞凋亡,ELISA法检测细胞炎症因子TNF-α、IL-1β的含量,Western blot检测细胞SOCS6、p-JAK2、p-STAT3蛋白表达。结果:SOCS6在hPDLFs细胞表达,随着LPS刺激,SOCS6基因表达下调,并且LPS浓度越高,细胞中SOCS6基因表达下调越明显。而且,hPDLFs细胞过表达SOCS6基因后,p-JAK2、p-STAT3蛋白表达明显降低,细胞炎症因子TNF-α、IL-1β含量减少,凋亡率下降。结论:SOCS6在LPS诱导的牙周炎细胞模型中表达下调,过表达SOCS6后细胞活力显著升高,凋亡率降低,此作用可能与抑制JAK2/STAT3信号通路及炎症因子IL-1β、TNF-α的表达有关。Objective:To explore the effects of SOCS6 on inflammation and apoptosis of human periodontal ligament fibroblasts(hPDLFs)through JAK2/STAT3 signaling pathway.Methods:hPDLFs in the logarithmic growth phase were divided into the following groups:control group,0.1 mg/L LPS group,1 mg/L LPS group,and 5 mg/L LPS group.qRT-PCR was used to observe the effect of LPS on the expression of SOCS6 mRNA in hPDLFs,Western blot was used to observe the effect of LPS on the expression of SOCS6 protein in hPDLFs,CCK-8 was used to observe the effect of LPS on the cell viability of hPDLFs,and ELISA was used to observe the effects of LPS on the inflammatory factors TNF-αand IL-1βof hPDLFs.The lentivirus titer,pre-experiment of the target cell infection,and cell transfection were detected,and SOCS6 mRNA expression was detected by qRT-PCR.hPDLFs in the logarithmic growth phase were transfected with overexpressed SOCS6.An inflammatory cell model of hPDLFs was then induced by LPS and treated overnight with the JAK2 signal activator coumermycin A1(CA1).The groups were as follows:LPS group(5 mg/L LPS),LPS+oe-NC group,LPS+oe-SOCS6 group,and LPS+oe-SOCS6+CA1 group.CCK-8 was used to detect cell viability in each group,flow cytometry was used to detect cell apoptosis in each group,ELISA was used to detect the contents of inflammatory factors TNF-αand IL-1β,and Western blot was used to detect the expression of SOCS6,p-JAK2,and p-STAT3 proteins.Results:SOCS6 was expressed in hPDLFs.With LPS stimulation,SOCS6 gene expression was down-regulated,and the higher the concentration of LPS,the more obvious the down-regulation of SOCS6 gene expression in cells.Moreover,after overexpression of SOCS6 gene in hPDLFs,the protein expression of p-JAK2 and p-STAT3 decreased obviously,the contents of inflammatory factors TNF-αand IL-1βdecreased,and the apoptosis rate decreased.Conclusion:The expression of SOCS6 is down-regulated in LPS-induced periodontitis cell model,and the cell viability is significantly increased and the apoptosis rate is decreased afte

关 键 词：细胞因子信号传导抑制因子6 JAK2/STAT3信号通路 人牙周膜成纤维细胞 TNF-Α IL-1Β 

分 类 号：R781.42[医药卫生—口腔医学]