ArticleJournal of pain research2021
Puerarin Attenuates Complete Freund's Adjuvant-Induced Trigeminal Neuralgia and Inflammation in a Mouse Model via Sirt1-Mediated TGF-β1/Smad3 Inhibition.
Article in Journal of pain research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.
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Who cites it
7 citing papers in PubMed, 1 synthesis or guideline pooled it, 10 citations in OpenAlex.
- A Systematic Review on Natural Products, Nanotechnology and their Recent Updates Towards Management of CFA-induced Rheumatoid Arthritis.Current drug discovery technologies · 2026Pooled it
- Efficacy of herbal medications in managing painful post-traumatic trigeminal neuropathy: a systematic review of studies in rodents.Frontiers in oral health · 2026Review
- Role of Chinese Medicine Monomers in Dry Eye Disease: Breaking the Vicious Cycle of Inflammation.Pharmacology research & perspectives · 2025Review
- From Plant to Chemistry: Sources of Antinociceptive Non-Opioid Active Principles for Medicinal Chemistry and Drug Design.Molecules (Basel, Switzerland) · 2024Review
- Rodent behavior following a dural inflammation model with anti-CGRP migraine medication treatment.Frontiers in neurology · 2023Article
- Pharmacological Activity, Pharmacokinetics, and Clinical Research Progress of Puerarin.Antioxidants (Basel, Switzerland) · 2022Review
- Beneficial effects of natural flavonoids on neuroinflammation.Frontiers in immunology · 2022Review
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPuerarin, an active compound of radix puerariae, is a major compound used in Chinese herbal medicines and it has been well known for its pharmacological effects, including antioxidant, anti‑inflammatory, neuroprotective and cardioprotective properties. The aim of the present study was to determine the role of puerarin (Pue) in complete Freund's adjuvant (CFA)-induced trigeminal neuralgia (TN) and the effects of this compound on Sirt1 activity and on the progression of CFA-induced TN.
methodsMice were injected with CFA on the unilateral face to induce TN. A cell model of inflammation-associated TN was established by interleukin-1β (IL-1β; 10 ng/mL) and tumor necrosis factor-α (TNF-α; 50 ng/mL) stimulation of neurons. Reverse transcription-quantitative PCR and Western blot analyses were performed to analyze mRNA and protein expression levels in trigeminal ganglion and nerve cells. Terminal-deoxynucleotidyl transferase mediated nick end labeling (TUNEL) staining was used to determine nerve cell apoptosis following IL-1β/TNF-α or Pue treatment.
resultsPue is a conceivable Sirtuin1 (Sirt1) activator used for the prevention of trigeminal nerve injury that attenuates CFA-induced TN and inflammatory cytokine-evoked overactivation of neuronal inflammation and apoptosis. Treatment of mice with inflammatory cytokines induced upregulation of cleaved caspase-3 protein expression, which was neutralized by Pue supplementation. Both in vivo and in vitro experiments led to the conclusion that Pue modulated Sirt1 activation and repressed transforming growth factor-β1 (TGF-β1) protein expression and drosophila mothers against decapentaplegic homolog3 (Smad3) phosphorylation in order to exert neuroprotection.
conclusionThe findings suggested that Pue functioned as a potential Sirt1 activator to improve neuroinflammation-induced TN and neuronal apoptosis via the suppression of TGF-β1/Smad3 activity. The pharmacological activity of Pue provides a new perspective for the effective prevention and treatment of TN.
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