Pain is a significant problem worldwide that affects the quality of life of patients.
Dezocine is a non-addictive
analgesic drug with kappa-
opioid antagonist activity and has been successfully used to alleviate of
postoperative pain. In addition,
dezocine has an
analgesic effect similar to that of
morphine, alleviating moderate to severe
pain. Rap
guanine nucleotide exchange factor 3 (RAPGEF3) is a
guanine nucleotide exchange factor for
GTPases Rap1 and Rap2, which could enhance the activity of Rap1 to promote cell adhesion and axon regeneration, as well as promote neurite extension by interacting with
nerve growth factors. Here, we first observed that overexpression of RAPGEF3 increased cell viability, as shown by a
CCK-8 assay, and recovered brain function in rats. The expression of
inflammation-related factors at the
mRNA level was detected using qPCR, and the concentration of these factors in a cultured cell medium and rat serum samples were decreased as shown by ELISA after RAPGEF3 overexpression. Through western blotting, we further found that pro-inflammatory
proteins were decreased, and these effects might be mediated by inhibition of the Ras/p-38 MAPK signaling pathway. Taken together, we speculated that RAPGEF3overexpression enhances the
therapeutic effect of
dezocine on
neuropathic pain by inhibiting the inflammatory response through inhibition of the Ras/p-38 MAPK signaling pathway.