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Pyruvate kinase M2 (PKM2), the key enzyme of glycolysis, is potentially implicated in periodontitis pathogenesis, although its precise role is unclear. Ginsenoside compound K (CK) has strong anti\u2010inflammatory effects. Prior studies indicate that CK down\u2010regulates PKM2 expression, yet it remains unclear whether CK can regulate PKM2 to modulate the inflammatory response. Furthermore, CK's role in periodontitis lacks pharmacological investigation.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      A periodontitis cell model was established by stimulating human gingival epithelial cells (HGECs) with\n                      <jats:italic>Porphyromonas gingivalis<\/jats:italic>\n                      (\n                      <jats:italic>Pg<\/jats:italic>\n                      ), and subsequently intervened with CK. Western blotting assessed the expressions of PKM2, phospho\u2010PKM2 (Tyr105), nuclear factor kappa\u2010B P65 (NF\u2010\u03baB P65), and phosphorylated NF\u2010\u03baB p65 (Ser536). Enzyme\u2010linked immunosorbent assay measured interleukin 1\u03b2 (IL\u20101\u03b2) and tumor necrosis factor\u2010\u03b1 (TNF\u2010\u03b1) levels in culture supernatants.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      <jats:italic>Pg<\/jats:italic>\n                      stimulation induced NF\u2010\u03baB p65 (Ser536) activation and the secretion of IL\u20101\u03b2 and TNF\u2010\u03b1 in HGECs and promoted PKM2 (Tyr105) phosphorylation. PKM2 was found to be the upstream regulator of NF\u2010\u03baB p65, and NF\u2010\u03baB p65 activated PKM2 through positive feedback to promote IL\u20101\u03b2 and TNF\u2010\u03b1 production, forming a feedback regulatory loop. CK inhibited\n                      <jats:italic>Pg<\/jats:italic>\n                      \u2010induced inflammation and NF\u2010\u03baB p65 (Ser536) and PKM2 (Tyr105) phosphorylation in HGECs. Furthermore, PKM2 overexpression significantly reversed CK's anti\u2010inflammatory effects.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>\n                      The PKM2\/NF\u2010\u03baB p65 pathway is involved in regulating the expression of inflammatory cytokines in\n                      <jats:italic>Pg<\/jats:italic>\n                      \u2010stimulated HGECs and serves as a crucial inflammatory regulatory pathway in the\n                      <jats:italic>Pg<\/jats:italic>\n                      \u2010stimulated HGECs model. CK exhibits anti\u2010inflammatory activity by inhibiting the PKM2\u2010mediated NF\u2010\u03baB signaling pathway and has potential as PKM2 modulator for treating periodontitis and other inflammatory diseases.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/omi.70029","type":"journal-article","created":{"date-parts":[[2026,4,2]],"date-time":"2026-04-02T04:25:49Z","timestamp":1775103949000},"page":"216-226","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Ginsenoside Compound K Plays an Anti\u2010Inflammatory Role in Gingival Epithelial Cells Stimulated With\n                    <i>Porphyromonas gingivalis<\/i>\n                    by Regulating Pyruvate Kinase M2"],"prefix":"10.1111","volume":"41","author":[{"ORCID":"https:\/\/orcid.org\/0009-0003-1933-4633","authenticated-orcid":false,"given":"Luxin","family":"Jin","sequence":"first","affiliation":[{"name":"School of Stomatology Kunming Medical University  Kunming Yunnan China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0004-1068-6066","authenticated-orcid":false,"given":"Lin","family":"Lu","sequence":"additional","affiliation":[{"name":"Institute of Biomedical Engineering Kunming Medical University  Kunming Yunnan China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9854-7762","authenticated-orcid":false,"given":"Yang","family":"Jiao","sequence":"additional","affiliation":[{"name":"Institute of Biomedical Engineering Kunming Medical University  Kunming Yunnan China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6404-1459","authenticated-orcid":false,"given":"Yanchun","family":"Wang","sequence":"additional","affiliation":[{"name":"Dentistry Department Dali University Health Science Center The First Affiliated Hospital of Dali University  Dali Yunnan China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1857-9925","authenticated-orcid":false,"given":"Hongbing","family":"He","sequence":"additional","affiliation":[{"name":"School and Hospital of Stomatology Kunming Medical University  Kunming Yunnan China"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2026,4,1]]},"reference":[{"key":"e_1_2_9_2_1","doi-asserted-by":"publisher","DOI":"10.1111\/prd.12362"},{"key":"e_1_2_9_3_1","doi-asserted-by":"publisher","DOI":"10.1111\/jre.12608"},{"key":"e_1_2_9_4_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.freeradbiomed.2019.08.007"},{"key":"e_1_2_9_5_1","doi-asserted-by":"publisher","DOI":"10.3389\/fimmu.2016.00145"},{"key":"e_1_2_9_6_1","doi-asserted-by":"publisher","DOI":"10.1186\/s12943-015-0490-2"},{"key":"e_1_2_9_7_1","doi-asserted-by":"publisher","DOI":"10.1177\/0022034521995157"},{"issue":"4","key":"e_1_2_9_8_1","first-page":"410","article-title":"Inflammaging: The Signaling Role of p65 Protein From the NF\u2010\u03baB Family]","volume":"37","author":"Belova Y. 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