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Abstract
Background
Dexmedetomidine (DEX) has showed significant analgesic effects in neuropathic pain, but the underlying mechanism has remained elusive. Our present study aimed to explore the effect of DEX on hyperalgesia with the involvement of p38MAPK signaling pathway in a rat model of monoarthritis (MA).
Methods
MA rat model was induced by injection of Complete Freund’s Adjuvant (CFA). Pathological changes of MA rats were observed by HE staining and Safranin-O/Fast Green staining. Ankle circumference, paw withdrawal latency (PWL) and paw withdrawal threshold (PWT) were measured to judge the degree of hyperalgesia in MA rats. Immunohistochemistry and ELISA were applied to observe the degree of inflammation in rats. Western blot analysis was conducted to detect expression of p38MAPK signaling pathway-related factors. The mechanism of p38MAPK signaling pathway in MA rats was observed via treatment of Anisomycin or SB203580 combined with DEX.
Results
After 8 h of CFA induction, joint swelling and hyperalgesia occurred in rats. There were obvious pathological changes in the joint cavity, the joint cavity space became narrow and synovial bursa became rough. A large number of inflammatory cell infiltration was observed under microscope. After injection of DEX and SB203580, PWT and PWL were prolonged, the expression of serum inflammatory factors was decreased, and the expression of p38MAPK signaling pathway-related factors was decreased; while all the detected indexes were recovered in MA rats after treated with DEX and Anisomycin.
Conclusions
Our study provided evidence that DEX could alleviate hyperalgesia in arthritis rats through inhibition of the p38MAPK signaling pathway.
Author contributions
BN is the the guarantor of integrity of the entire study; BN contributed to the study design and manuscript preparation; BN and QL contributed to the study concepts and experimental studies; BN and HJ contributed to the definition of intellectual content; BN, HJ and HC contributed to the literature research; HJ and HC contributed to the clinical studies; HC and QL contributed to the data acquisition; BN, HC and QL contributed to the data analysis; QL statistical analysis; All authors read and approved the final manuscript.
Disclosure statement
No potential conflict of interest was reported by the author(s).
Data availability statement
All the data generated or analyzed during this study are included in this published article.