热带农业科学2026，Vol.46Issue(1)：108-114,7.DOI:10.12008/j.issn.1009-2196.2026.01.016
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
Mitigative Effect of Epicatechin on LPS-Induced Inflammatory Injury in Periodontal Ligament Fibroblasts
摘要
Abstract
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.关键词
表儿茶素/人牙周膜成纤维细胞/细胞焦亡/NF-κB/LPSKey words
epicatechin,EC/human periodontal ligament fibroblasts/pyroptosis/NF-κB/LPS分类
医药卫生引用本文复制引用
吴煜,郝春波..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[J].热带农业科学,2026,46(1):108-114,7.基金项目
海南省重点研发项目(No.ZDYF2022SHFZ017). （No.ZDYF2022SHFZ017）
