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Peer-reviewedCC BY-NC-ND 4.0International Journal of Molecular Medicine

Multi-target mechanisms of paeoniflorin in inflammatory regulation: A network pharmacology (Review)

  • Jin Zhang1,2
  • Junjie Ye2
  • Kun Jin2
  • Xuan Sun1
  • Xinyu Yu1
  • Yuan Zhao3
  • Ni Zhu1,2
  1. 1School of Stomatology and Ophthalmology, Xianning Medical College, Hubei University of Science and Technology, Xianning, Hubei 437100, P.R. China
  2. 2Hubei Key Laboratory of Environmental Risks and Related Diseases Precision Control, School of Basic Medicine Sciences, Hubei University of Science and Technology, Xianning, Hubei 437100, P.R. China
  3. 3School of Biomedical Engineering, Xianning Medical College, Hubei University of Science and Technology, Xianning, Hubei 437100, P.R. China
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Abstract

Paeoniflorin (PF), a monoterpene glycoside from Paeonia roots, shows low toxicity and broad anti-inflammatory activity. A systematic review (PubMed, through 2025) with network pharmacology indicates that PF restores mitochondrial function, raises anti-inflammatory mediators (IL-10 and arginase-1), reduces TNF-α, IL-1β and IL-6, and eases oxidative stress. Its effects hinge on intertwined routes, dampening TLR4/MyD88, blocking NF-κB nuclear entry, lowering MAPK phosphorylation, reshaping JAK-STAT, and disrupting NLRP3 inflammasome assembly. Network mapping singles out a conserved core module (MAPK1, MAPK3, HSP90AA1, TP53, ESR1, BCL2, HIF1A, IL6, IL10 and FGF2), with HSP90AA1 and ESR1 as disease-tailored effectors in rheumatoid arthritis and osteoarthritis (OA). PF absorbs fast and gathers in the liver with minimal toxicity, yet oral availability stays poor. Preclinical promise spans OA, colitis, and atherosclerosis, while clinical data remain thin. Synergistic pairing with other agents and structural refinement of PF broaden its reach, though such computational leads need experimental corroboration. Future efforts should improve its bioavailability, develop targeted delivery systems, and conduct rigorous clinical trials to move PF from tradition to evidence-based medicine.

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Cite

BibTeXRIS
BibTeX
@article{zhang2026multitarget,
  title = {{Multi-target mechanisms of paeoniflorin in inflammatory regulation: A network pharmacology (Review)}},
  author = {Jin Zhang and Junjie Ye and Kun Jin and Xuan Sun and Xinyu Yu and Yuan Zhao and Ni Zhu},
  journal = {International Journal of Molecular Medicine},
  year = {2026},
  month = oct,
  doi = {10.3892/ijmm.2026.6010},
  url = {https://doi.org/10.3892/ijmm.2026.6010},
  note = {CC BY-NC-ND 4.0},
}
RIS
TY  - JOUR
TI  - Multi-target mechanisms of paeoniflorin in inflammatory regulation: A network pharmacology (Review)
AU  - Jin Zhang
AU  - Junjie Ye
AU  - Kun Jin
AU  - Xuan Sun
AU  - Xinyu Yu
AU  - Yuan Zhao
AU  - Ni Zhu
PY  - 2026
DA  - 2026/10/09
JO  - International Journal of Molecular Medicine
DO  - 10.3892/ijmm.2026.6010
UR  - https://doi.org/10.3892/ijmm.2026.6010
AB  - Paeoniflorin (PF), a monoterpene glycoside from Paeonia roots, shows low toxicity and broad anti-inflammatory activity. A systematic review (PubMed, through 2025) with network pharmacology indicates that PF restores mitochondrial function, raises anti-inflammatory mediators (IL-10 and arginase-1), reduces TNF-α, IL-1β and IL-6, and eases oxidative stress. Its effects hinge on intertwined routes, dampening TLR4/MyD88, blocking NF-κB nuclear entry, lowering MAPK phosphorylation, reshaping JAK-STAT, and disrupting NLRP3 inflammasome assembly. Network mapping singles out a conserved core module (MAPK1, MAPK3, HSP90AA1, TP53, ESR1, BCL2, HIF1A, IL6, IL10 and FGF2), with HSP90AA1 and ESR1 as disease-tailored effectors in rheumatoid arthritis and osteoarthritis (OA). PF absorbs fast and gathers in the liver with minimal toxicity, yet oral availability stays poor. Preclinical promise spans OA, colitis, and atherosclerosis, while clinical data remain thin. Synergistic pairing with other agents and structural refinement of PF broaden its reach, though such computational leads need experimental corroboration. Future efforts should improve its bioavailability, develop targeted delivery systems, and conduct rigorous clinical trials to move PF from tradition to evidence-based medicine.
SN  - 1107-3756
SN  - 1791-244X
ER  -