摘要
目的探究黄芩苷对脂多糖(LPS)诱导的人牙周膜干细胞(hPDLSCs)增殖、迁移及Janus蛋白酪氨酸激酶2(JAK2)/信号转导和转录激活因子3(STAT3)信号通路的调控作用。方法将hPDLSCs分为对照组、LPS组、黄芩苷不同浓度(0.1、1、10 mg/L)组,采用ELISA法和CCK-8法测定细胞炎症因子[白细胞介素6(IL-6)、IL-1β和肿瘤坏死因子α(TNF-α)]含量和细胞活力,以筛选最适黄芩苷浓度并进行后续通路验证实验。随后将细胞分为对照组、LPS组、最适黄芩苷浓度组、抑制剂组(10μg/mL LPS+1 mg/L黄芩苷+3μmol/L JAK2/STAT3通路抑制剂AG490),干预24 h后检测hPDLSCs增殖率、凋亡率、迁移率、侵袭细胞数、细胞周期素D1(Cyclin D1)、胱天蛋白酶3(caspase-3)mRNA和蛋白表达及JAK2/STAT3信号通路相关蛋白表达。结果根据细胞炎症因子含量和细胞活力结果选择1 mg/L为黄芩苷最适浓度。与对照组比较,LPS组细胞增殖率、迁移率、侵袭细胞数、Cyclin D1 mRNA及蛋白表达水平显著降低,细胞凋亡率、caspase-3 mRNA及蛋白表达、p-JAK2和p-STAT3蛋白表达显著升高(P<0.05);经1 mg/L黄芩苷干预后,上述指标均得到显著改善(P<0.05);而抑制剂组上述指标的改善程度更加显著(P<0.05)。结论黄芩苷可通过抑制JAK2/STAT3信号通路来促进LPS诱导的h PDLSCs增殖、迁移和侵袭,抑制其凋亡及炎症反应。
OBJECTIVE To explore the regulatory effects of baicalin on the proliferation and migration of human periodontal ligament stem cells(hPDLSCs)induced by lipopolysaccharide(LPS)and Janus protein tyrosine kinase 2(JAK2)/signal transduction and transcription activator 3(STAT3)signaling pathways.METHODS hPDLSCs were divided into control group,LPS group,different concentration baicalin groups(0.1,1 and 10 mg/L).ELISA method and CCK-8 assay were used to determine the contents of cell inflammatory factors[interleukin 6(IL-6),IL-1βand tumor necrosis factor-α(TNF-α)]and cell viability,so as to screen the optimal concentration of baicalin for follow-up pathway validation experiments.The cells were then divided into control group,LPS group,optimal baicalin concentration group and inhibitor group(10μg/mL LPS+1 mg/L baicalin+3μmol/L JAK2/STAT3 pathway inhibitor AG490).After treated for 24 h,the proliferation rate of hPDLSCs,apoptosis rate,migration rate,invasion cell number,mRNA and protein expressions of Cyclin D1 and caspase-3,the expression of JAK2/STAT3 pathway-related proteins were all detected.RESULTS According to cell inflammatory factors and cell viability,1 mg/L was selected as the optimal concentration of baicalin.Compared with control group,cell proliferation rate,migration rate,invasion cell number,Cyclin D1 mRNA and protein expression were significantly decreased in LPS group,while cell apoptosis rate,caspase-3 mRNA and protein expression,p-JAK2 and p-STAT3 protein expression were significantly increased(P<0.05).After treated with 1 mg/L baicalin,the above indexes were reversed significantly(P<0.05).The improvement of above indexes in the inhibitor group was more obvious(P<0.05).CONCLUSIONS Baicalin can promote the proliferation,migration and invasion of LPS-induced hPDLSCs and inhibit their apoptosis and inflammation by blocking the JAK2/STAT3 pathway.
作者
王桥
冯博
高永志
WANG Qiao;FENG Bo;GAO Yongzhi(Dept.of Stomatology,the Second Affiliated Hospital of Qiqihar Medical College,Heilongjiang Qiqihar 161006,China;Dept.of Stomatology,Qiqihar Wuguan Hospital,Heilongjiang Qiqihar 161006,China;Dept.of Stomatology,the First Affiliated Hospital of Qiqihar Medical College,Heilongjiang Qiqihar 161041,China)
出处
《中国药房》
CAS
北大核心
2023年第10期1216-1222,共7页
China Pharmacy
基金
黑龙江省省属高等学校基本科研业务费科研项目(No.2021-KYYWF-0374)。
关键词
牙周炎
黄芩苷
牙周膜干细胞
Janus蛋白酪氨酸激酶2/信号转导和转录激活因子3信号通路
增殖
迁移
periodontitis
baicalin
periodontal ligament stem cells
Janus protein tyrosine kinase 2/signal transduction and transcription activator 3 signaling pathway
proliferation
migration
