Evidence map›Paper›PMID 42871523›Full record

ArticleFrontiers in pharmacology2026

A Yeong Lee, Su-Bin Park, Eunjung Son, Junghyun Kim, Dong-Seon Kim, Soon Yeong Park, Hyeri Ku, Jung-In Kim, Yun Mi Lee

Abstract read
In one paragraph

Article in Frontiers in pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors.

A Yeong LeeKM Data Division, Korea Institute of Oriental Medicine, Daejeon, Republic of Korea.
Su-Bin ParkDepartment of Oral Pathology, School of Dentistry, Jeonbuk National University, Jeonju, Republic of Korea.
Eunjung SonKM Science Research Division, Korea Institute of Oriental Medicine, Daejeon, Republic of Korea.
Junghyun KimDepartment of Oral Pathology, School of Dentistry, Jeonbuk National University, Jeonju, Republic of Korea.
Dong-Seon KimKM Science Research Division, Korea Institute of Oriental Medicine, Daejeon, Republic of Korea.
Soon Yeong ParkCNS Pharm Korea Co., Ltd., Seoul, Republic of Korea.
Hyeri KuCNS Pharm Korea Co., Ltd., Seoul, Republic of Korea.
Jung-In KimCNS Pharm Korea Co., Ltd., Seoul, Republic of Korea.
Yun Mi LeeKM Science Research Division, Korea Institute of Oriental Medicine, Daejeon, Republic of Korea.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: This study was conducted to investigate the preventive effects of Methods: The protective effects of PBE were evaluated in a lipopolysaccharide (LPS)-induced periodontitis rat model by assessing histological changes, TRAP-positive osteoclast presence, and alveolar bone loss. Network pharmacology, protein-protein interaction network analysis, KEGG pathway enrichment analysis, and molecular docking were performed to predict the potential targets and mechanisms of PBE. The anti-inflammatory effects of PBE were further investigated in RAW264.7 macrophages and human periodontal ligament fibroblasts (PDLFs). Inflammatory mediators, cytokines, matrix metalloproteinases (MMPs), and PI3K/Akt/NF-κB signaling-related proteins were analyzed. Major constituents of PBE were identified using UPLC-QTOF-MS, and their anti-inflammatory activities were evaluated Results: 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 Conclusion: 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

Indexed as

flavonoid glucuronidemolecular dockingnetwork pharmacologyNF-κBperiodontitisPI3K/AKT signalingPimpinella brachycarpa

Identifiers

PMID42871523
PMCPMC13658597

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.