Blocking of Caveolin-1 Attenuates Morphine-Induced Inflammation, Hyperalgesia, and Analgesic Tolerance Via Inhibiting NLRP3 Inflammasome and ERK/c-JUN Pathway
Overview
Authors
Affiliations
Morphine is generally used to treat chronic pain in clinic. But long-term use of morphine can inevitably induce analgesic tolerance and hyperalgesia. Caveolin-1 is reported to affect morphine-mediated signaling transduction. However, the action mechanism of morphine-induced analgesic tolerance is still unknown. In this study, morphine-induced analgesic tolerance model was established in Sprague-Dawley rats. The effects of Caveolin-1 blocking on neuroinflammation and ERK/c-JUN pathway were then explored. Morphine can remarkably elevate the expression level of Caveolin-1. Based on paw withdrawal latency behavior test, we found that Caveolin-1 blocking can effectively attenuate morphine-induced analgesic tolerance and neuroinflammation. Activation of ERK/c-JUN significantly reversed the above influences caused by Caveolin-1 blocking. Taken together, blocking of Caveolin-1 can attenuate morphine-induced inflammation and analgesic tolerance through inhibiting NLRP3 inflammasome and ERK/c-JUN pathway.
Caveolin-1 regulates inflammatory mediators in retinal endothelial cells.
Jiang Y, Liu L, Al-Shabrawey M, Steinle J Mol Vis. 2025; 30:298-303.
PMID: 39959177 PMC: 11829789.
Li H, Yang Z, Liang W, Nie H, Guan Y, Yang N J Gerontol A Biol Sci Med Sci. 2024; 79(4).
PMID: 38407305 PMC: 10949436. DOI: 10.1093/gerona/glae059.
Molavinia S, Nikravesh M, Pashmforoosh M, Rajabi Vardanjani H, Khodayar M Neurochem Res. 2023; 49(2):415-426.
PMID: 37864024 DOI: 10.1007/s11064-023-04043-2.