Table 1_Pimpinella brachycarpa extract attenuates periodontal inflammation by modulating the PI3K/Akt–NF-κB signaling pathway.xlsx

Major constituents of PBE were identified using UPLC-QTOF-MS, and their anti-inflammatory activities were evaluated in vitro.</p>Results<p>PBE attenuated periodontal tissue destruction in LPS-induced periodontitis rats, as demonstrated by reduced inflammatory cell infiltration, decreased CEJ–ABC distance, and suppression of TRAP-positive osteoclast presence. Network pharmacology analysis identified the PI3K/Akt signaling pathway as a key target associated with the anti-inflammatory effects of PBE.

In RAW264.7 macrophages, PBE significantly reduced the production of NO, PGE2, TNF-α, and IL-1β. In PDLFs, PBE suppressed IL-1β-induced production of PGE2, IL-6, and IL-1β and downregulated the expression of MMP-3, MMP-8, and MMP-13. Furthermore, PBE inhibited the phosphorylation of PI3K, Akt, IKK, IκBα, and NF-κB p65.

Chemical profiling identified chlorogenic acid, luteolin 7-O-glucuronide, apigenin 7-O-glucuronide, and luteolin 3′-O-glucuronide as major constituents. Among these, flavonoid glucuronides exhibited stronger anti-inflammatory activities than chlorogenic acid in vitro.</p>Conclusion<p>The present findings indicate that PBE exerts anti-inflammatory and tissue-protective effects in experimental models of periodontitis. The observed effects were associated with suppression of PI3K/Akt–NF-κB signaling.

In addition, flavonoid glucuronides identified in PBE exhibited anti-inflammatory activities in vitro. Further studies are required to clarify the contribution of individual constituents to the biological activity of PBE.</p>