遵义医科大学学报2025，Vol.48Issue(4)：332-338,7.
异欧前胡素对脂多糖诱导牙周膜成纤维细胞损伤的调节作用机制
The protective effects of isoimperatorin on lipopolysaccharide induced damage in periodontal ligament cells
摘要
Abstract
Objective To investigate the effects of isoimperatorin on lipopolysaccharide(LPS)induced damage in human periodontal ligament cells(hPDLCs)and the possible mechanism.Methods LPS(5 mg/L)was used to induce inflammation in hPDLCs for 24 hours.LPS-induced hPDLCs were treated with isoimperatorin at differ-ent concentrations for 48 hours.Cell viability of hPDLCs was detected with CCK-8 assay.Cell apoptosis was e-valuated by TUNEL staining.The levels of SOD,GSH,MDA,MPO,IL-1β,IL-6,IL-18,MCP-1 and TNF-α were determined by ELISA assay.The expression levels of p-IκBα,p-p65,p-ERK were detected by Western blot.Results Compared with LPS-induced hPDLCs,cell viability was significantly improved after indicated treat-ments of isoimperatorin in a dose-dependent manner(P＜0.01).LPS treatment increased apoptotic cells,while isoimperatorin decreased cell apoptosis(P＜0.01).The levels of SOD and GSH in LPS-induced hPDLCs were reduced,and the levels of MDA and MPO were increased(P＜0.001).The levels of SOD,GSH,MDA,and MPO in LPS-induced hPDLCs with treatment of isoimperatorin were significantly reversed in a dose-dependent manner(P＜0.001).The expression levels of IL-1β,IL-6,IL-18,MCP-1,and TNF-αin LPS-induced hPDLCs were significantly increased,and isoimperatorin treatment significantly reduced the levels of IL-1β,IL-6,IL-18,MCP-1,and TNF-αin LPS-damaged hPDLCs(P＜0.001).The expression levels of p-IκBα,p-p65,p-ERK were increased,and isoimperatorin inhibited the elevation of these proteins(P＜0.001).Conclusion Cell apoptosis,oxidative stress and inflammation in LPS-induced hPDLCs were inhibited with isoimperatorin treatment,probably by regulating ERK and NF-κB signaling pathways.关键词
异欧前胡素/人牙周膜成纤维细胞/ERK/NF-κB信号通路Key words
isoimperatorin/human periodontal ligament cells fibroblast/ERK/NF-κB signaling pathway分类
口腔医学引用本文复制引用
杨艳,张楠,李娜..异欧前胡素对脂多糖诱导牙周膜成纤维细胞损伤的调节作用机制[J].遵义医科大学学报,2025,48(4):332-338,7.基金项目
山西省基础研究计划项目(NO:202103021224359). （NO:202103021224359）
