表儿茶素对脂多糖(LPS)诱导的牙周膜成纤维细胞炎性损伤的缓解作用OA
Mitigative Effect of Epicatechin on LPS-Induced Inflammatory Injury in Periodontal Ligament Fibroblasts
探讨海南特色植物源小分子化合物表儿茶素(Epicatechin,EC)对脂多糖(LPS)诱导的人牙周膜成纤维细胞(hPDLFs)炎性损伤的保护作用及其分子机制.采用 MTT法检测表儿茶素对 hPDLFs活性的影响,使用 LPS构建细胞炎症模型,通过 qPCR 和 ELISA 检测炎性因子(IL-1β、IL-6、TNF-α、IL-8)表达.利用 Western blot 分析NLRP3/Caspase-1/GSDMD焦亡通路及NF-κB信号通路关键蛋白(p-p65、p65)表达,通过核质分离实验观察p-p65 核转位情况.结果表明:EC在 1 和 2 μmol/L浓度下对hPDLFs无细胞毒性,但显著抑制LPS诱导的炎性因子mRNA表达及蛋白水平升高(p<0.05);机制研究表明,EC可下调NLRP3、Caspase-1 及GSDMD-N蛋白表达,同时抑制NF-κB通路P65 亚基和IkBα磷酸化,并阻断其核转位这一过程(p<0.05).EC通过双重调控NLRP3 炎性小体介导的细胞焦亡及NF-κB信号通路活化,拮抗LPS诱导的hPDLFs炎性损伤,其靶向抑制p65 磷酸化核转位的作用模式为牙周炎治疗提供了新策略.
This study aimed to explore the protective effect and molecular mechanism of epicatechin(EC),a small-molecule compound derived from Hainan characteristic plants,against lipopolysaccharide(LPS)-induced inflammatory injury in human periodontal ligament fibroblasts(hPDLFs).The MTT assay was used to detect the effect of epicatechin on the activity of hPDLFs,and LPS was used to construct a cellular inflammation model.The expression of inflammatory factors(IL-1β,IL-6,TNF-α,and IL-8)was detected by qPCR and ELISA.Western blotting was employed to analyze the expression of key proteins in the NLRP3/Caspase-1/GSDMD pyroptosis pathway and the NF-κB signaling pathway(p-p65,p65),and the nuclear trans-location of p-p65 was observed through a nuclear-cytoplasmic fractionation assay.The results showed that EC at concentra-tions of 1 and 2 μmol·L-1 had no cytotoxicity to hPDLFs,but significantly inhibited the LPS-induced increases in the mRNA expression and protein levels of inflammatory factors(p<0.05).Mechanistic studies indicated that EC could downregulate the expression of NLRP3,Caspase-1,and GSDMD-N proteins and simultaneously inhibit the phosphorylation of the p65 subunit and IκBα in the NF-κB pathway and block the process of their nuclear translocation(p<0.05).EC antagonizes LPS-induced inflammatory injury in hPDLFs by dual regulation of NLRP3 inflammasome-mediated pyroptosis and the activation of the NF-κB signaling pathway.Its mode of action,targeting the inhibition of p65 phosphorylation and nuclear translocation,pro-vides a new strategy for the treatment of periodontitis.
吴煜;郝春波
海南医科大学附属海南医院(海南省人民医院) 海南 海口 571199||海南科技职业大学医药学院 海南 海口 571126海南医科大学附属海南医院(海南省人民医院) 海南 海口 571199
医药卫生
表儿茶素人牙周膜成纤维细胞细胞焦亡NF-κBLPS
epicatechin,EChuman periodontal ligament fibroblastspyroptosisNF-κBLPS
《热带农业科学》 2026 (1)
108-114,7
海南省重点研发项目(No.ZDYF2022SHFZ017).
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