Scholarlink

<p>This study aimed to elucidate the anti-inflammatory mechanisms of Platycodon grandiflorum extract (PGE) in periodontitis through an integrated approach combining network pharmacology and experimental validation. Potential active compounds and targets of PGE were identified using database mining, protein–protein interaction, and enrichment analyses, followed by molecular docking. The anti-inflammatory effects of PGE were evaluated in Porphyromonas gingivalis lipopolysaccharide (Pg-LPS)-stimulated RAW264.7 macrophages using CCK-8, Griess, ELISA, and Western blot assays. Network analysis identified TP53, TNF, JUN, IL6, and AKT1 as key targets enriched in NF-κB, MAPK, and AKT signaling pathways. PGE significantly reduced Pg-LPS-induced production of NO, TNF-α, IL-6, IL-1β, iNOS, and COX-2, and suppressed the activation of NF-κB, MAPK (p38, ERK1/2, JNK), and AKT signaling pathways by inhibiting their phosphorylation, without obvious cytotoxicity. PGE exerts potent anti-inflammatory activity in Pg-LPS–induced macrophages, at least partly by inhibiting the NF-κB, p38, ERK1/2, JNK, and AKT signaling pathways, providing mechanistic support for its potential application in periodontitis management.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Mechanistic investigation of the anti-inflammatory effects of platycodon grandiflorum extract in periodontitis based on network pharmacology and experimental validation

  • 期刊论文

  • 发表日期：

    2026年5月21日

查看全文
  • Xiaoling Xu,
  • Minjuan Pan,
  • Wei Zhang,
  • Bin Hu

摘要

This study aimed to elucidate the anti-inflammatory mechanisms of Platycodon grandiflorum extract (PGE) in periodontitis through an integrated approach combining network pharmacology and experimental validation. Potential active compounds and targets of PGE were identified using database mining, protein–protein interaction, and enrichment analyses, followed by molecular docking. The anti-inflammatory effects of PGE were evaluated in Porphyromonas gingivalis lipopolysaccharide (Pg-LPS)-stimulated RAW264.7 macrophages using CCK-8, Griess, ELISA, and Western blot assays. Network analysis identified TP53, TNF, JUN, IL6, and AKT1 as key targets enriched in NF-κB, MAPK, and AKT signaling pathways. PGE significantly reduced Pg-LPS-induced production of NO, TNF-α, IL-6, IL-1β, iNOS, and COX-2, and suppressed the activation of NF-κB, MAPK (p38, ERK1/2, JNK), and AKT signaling pathways by inhibiting their phosphorylation, without obvious cytotoxicity. PGE exerts potent anti-inflammatory activity in Pg-LPS–induced macrophages, at least partly by inhibiting the NF-κB, p38, ERK1/2, JNK, and AKT signaling pathways, providing mechanistic support for its potential application in periodontitis management.