ArticleInternational journal of immunopathology and pharmacology
Rapamycin ameliorates inflammatory pain via recovery of autophagy flux mediated by mammalian target of rapamycin (mTOR) signaling pathway in the rat spinal cord.
Article in International journal of immunopathology and pharmacology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed.
- Betanin fromBiomedicines · 2026Article
- Electroacupuncture Attenuates Cyclophosphamide-Induced Bladder Pain by Restoring Autophagy in Spinal Inhibitory Interneurons.ACS omega · 2026Article
- Cold receptor TRPM8 as a target for migraine-associated pain and affective comorbidities.The journal of headache and pain · 2025Article
- PDCD4 inhibition alleviates neuropathic pain by regulating spinal autophagy and neuroinflammation.Molecular painArticle
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9 authors.
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Abstract
objectiveThis study aimed to investigate the effect of rapamycin on inflammatory pain in rats.
introductionInflammatory pain is a kind of pathological pain caused by inflammatory mediators or factors such as TNF-α (Tumor Necrosis Factor-α), IL-1β (Interleukin-1β), and IL-6 (Interleukin-6). NSAIDs and opioid analgesics are commonly used for relieving inflammatory pain, but the side effects limit their clinical application. New drugs based on new mechanisms for inflammatory pain are urgently needed. Autophagy is an evolutionarily conserved homeostatic process for lysosomal degradation of intracellular components. Recent reports indicate the involvement of autophagy in the development and maintenance of neuropathic pain, but the role of autophagy in inflammatory pain still needs to be explored.
methodsThe pain-related behaviors of rats were studied by paw withdrawal threshold and paw withdrawal latency. The autophagy level of the rat spinal cord was detected by western blots. The concentrations of TNF-α, IL-1β, and IL-6 were detected by ELISA.
resultsWe found that the paw withdrawal threshold and paw withdrawal latency were both significantly decreased after CFA (Complete Freund's Adjuvant) injection, accompanied by the activation of mTOR signaling pathway and the inhibited autophagy flux in the spinal cord. And inflammatory cytokines were increased in the spinal cord after CFA injection. Then, we studied the effect of rapamycin on CFA-induced inflammatory pain in rats, and found that rapamycin restored the autophagy flux and significantly reduced mechanical allodynia and thermal hyperalgesia. In addition, rapamycin significantly decreased the levels of TNF-α, IL-1β, and IL-6 after CFA injection in the spinal cord.
conclusionOur results suggested that rapamycin might be a promising candidate for the treatment of inflammatory pain by restoring the autophagy flux in the spinal cord.
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