Combined Effects of Puerarin and Adipose-Derived Stem Cells on Alveolar Bone Preservation and Inflammation Control in Periodontitis Through p38MAPK Modulation.
Yang T., Zhang X., Zhang LF.
Animal Study on Chronic Inflammation, published in Kaohsiung J Med Sci (2026) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Animal Study
- Journal
- Kaohsiung J Med Sci (2026)
- Country
- China (Republic : 1949- )
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 41631577
- DOI
- 10.1002/kjm2.70182
Abstract (original English)
This study evaluated the effects of puerarin and adipose-derived stem cells (ADSCs), alone or combined, on p38MAPK activity, alveolar bone preservation, and inflammatory responses in a rat periodontitis (PD) model and in vitro. ADSCs were exposed to various puerarin concentrations to assess cell proliferation, osteogenic differentiation, and p38MAPK-related protein expression. Additional experiments employed anisomycin (a p38 MAPK activator) and Porphyromonas gingivalis LPS (Pg-LPS) to determine whether puerarin attenuates p38MAPK overactivation and reduces pro-inflammatory cytokine production. In vivo, ligature- and Porphyromonas gingivalis-induced periodontitis rats were randomized to Normal, PD, PD + ADSCs, PD + puerarin, or PD + puerarin + ADSCs groups, and alveolar bone microarchitecture (micro-CT) and periodontal p38MAPK activation and osteogenic/inflammatory proteins (Western blot, ELISA) were assessed. At 10 -6 M, puerarin significantly increased ADSC proliferation and osteogenic differentiation, whereas anisomycin activation diminished these benefits, which were restored by co-treatment with puerarin. Puerarin also reduced Pg-LPS induced secretion of pro-inflammatory cytokines by suppressing p38MAPK. In vivo, the periodontitis group showed substantial alveolar bone loss and marked inflammatory cell infiltration. Both ADSCs and puerarin partially alleviated these change
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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