ArticleMolecular neurobiology2026
Study on the Analgesic Mechanism of Aloperine in Mice with Neuropathic Pain Based on the p38MAPK/FKN/CX3CR1 Pathway.
Article in Molecular neurobiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
A lesion or disease of the somatosensory nervous system causes neuropathic pain (NP). Previous experiments have demonstrated that aloperine (ALO) exhibits antiallodynic effects on neuropathic pain in mice; however, the mechanism underlying its analgesic action remains unclear. This study investigated the analgesic mechanism of ALO on neuropathic pain in mice using a chronic constriction injury (CCI) model. Experiments were conducted using the ALO and p38MAPK inhibitor SB 203580. In vivo experiments demonstrated that ALO played an analgesic role by inhibiting p38MAPK phosphorylation, and it improved mechanical allodynia, cold allodynia, and hot hyperalgesia in CCI mice, as well as having a protective effect on injured sciatic nerves. The combined administration of a subthreshold dose of ALO (20 mg/kg) with the p38MAPK inhibitor SB203580 (20 mg/kg) produced significant analgesic effects, suggesting that ALO likely shares a common target with SB203580, namely p38MAPK. Fluorescence double staining indicated that the antiallodynic effect of ALO may be related to its inhibition of the p38MAPK/FKN/CX3CR1 pathway in the spinal cord, and it may play a role in regulating the expression of p38MAPK in microglial cells. In vitro studies have shown that ALO can reduce the activation of BV
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