ArticleFrontiers in molecular neuroscience2023
Resveratrol suppresses neuroinflammation to alleviate mechanical allodynia by inhibiting Janus kinase 2/signal transducer and activator of transcription 3 signaling pathway in a rat model of spinal cord injury.
Article in Frontiers in molecular neuroscience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.
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Who cites it
8 citing papers in PubMed, 1 synthesis or guideline pooled it, 10 citations in OpenAlex.
- Protective effect and possible mechanisms of resveratrol in animal models of spinal cord injury: a preclinical systematic review and meta-analysis.Frontiers in immunology · 2026Pooled it
- STAT3 Signaling in Spinal Cord Injury: Neurochemical Mechanisms Linking Neuroinflammation, Mitochondrial Stress, and Glial Remodeling.Neurochemical research · 2026Review
- Resveratrol therapy modulates inflammatory biomarkers and reverses mechanical allodynia in rats subjected to a temporomandibular joint arthritis model.Inflammopharmacology · 2026Article
- Dihydro-R demonstrates innate immunity against Adenovirus-7 by suppressing the NF-κB/JAK-STAT pathway in a SIRT1-dependent manner.Biochemistry and biophysics reports · 2026Article
- Resveratrol: Harnessing Nature's Potential for Chronic Pain Relief.Aging and disease · 2025Review
- The Potential Application of Resveratrol and Its Derivatives in Central Nervous System Tumors.International journal of molecular sciences · 2024Review
- RNA Interference Unleashed: Current Perspective of Small Interfering RNA (siRNA) Therapeutics in the Treatment of Neuropathic Pain.ACS pharmacology & translational science · 2024Review
- Progress in treatment of pathological neuropathic pain after spinal cord injury.Frontiers in neurology · 2024Review
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Neuropathic pain (NP) is one of intractable complications of spinal cord injury (SCI) and lacks effective treatment. Resveratrol (Res) has been shown to possess potent anti-inflammatory and anti-nociceptive effects. In this study, we investigated the analgesic effect of Res and its underlying mechanism in a rat model of SCI. Methods: The rat thoracic (T10) spinal cord contusion injury model was established, and mechanical thresholds were evaluated during an observation period of 21 days. Intrathecal administration with Res (300 μg/10 μl) was performed once a day for 7 days after the operation. On postoperative day 7, the expressions of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and interleukin-6 (IL-6) were determined by enzyme-linked immunosorbent assay (ELISA) and Real-time quantitative PCR (RT-qPCR), the expression of Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) signaling pathway was determined by western blot and RT-qPCR, and the co-labeled phospho-STAT3 (p-STAT3) with neuronal nuclear antigen (NeuN), glial fibrillary acidic protein (GFAP), and ionized calcium-binding adapter molecule 1 (Iba-1) were explored by double immunofluorescence staining in the lumbar spinal dorsal horns. The temporal changes of p-STAT3 were investigated by western blot on the 1st, 3rd, 7th, 14th, and 21st days after the operation. Results: Intrathecal administration with Res for 7 successive days alleviated mechanical allodynia of rats during the observation period. Meanwhile, treatment with Res suppressed the production of pro-inflammatory factors TNF-α, IL-1β and IL-6, and inhibited the expressions of phospho-JAK2 and p-STAT3 in the lumbar spinal dorsal horns on postoperative day 7. Additionally, the protein expression of p-STAT3 was significantly increased on the 1st day following the operation and remained elevated during the next 21 days, immunofluorescence suggested that the up-regulated p-STAT3 was co-located with glial cells and neurons. Conclusion: Our current results indicated that intrathecal administration with Res effectively alleviated mechanical allodynia after SCI in rats, and its analgesic mechanism might be to suppress neuroinflammation by partly inhibiting JAK2/STAT3 signaling pathway.
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