Aim of the study
This study aimed to evaluate the analgesic effect of SGE on complete Freund's adjuvant (CFA)-induced inflammatory pain rats, and to investigate whether its effect on relieving inflammatory pain is associated with regulation of P2X3 receptor. Materials and
Conclusions
In summary, our research indicated that SGE could alleviate CFA-induced inflammatory pain by suppression of P2X3 receptor.
Methods
The analgesic effects of SGE on CFA-induced inflammatory pain rats were evaluated by measuring mechanical pain threshold, thermal pain threshold, and motor coordination ability. The mechanisms of SGE in relieving inflammatory pain were explored by detecting inflammatory factors levels, NF-κB, COX-2 and P2X3 expression, and were further verified by addition of P2X3 receptor agonist (α, β me-ATP).
Results
Our results revealed that SGE can notably increase the mechanical pain threshold and thermal pain threshold of CFA-induced inflammatory pain rats, and markedly alleviate the pathological damage in DRG. SGE could suppress the release of inflammatory factors including IL-1β, IL-6, TNF-α and restrain the expression of NF-κB, COX-2 and P2X3. Moreover, α, β me-ATP further exacerbated the inflammatory pain of CFA-induced rats, while SGE could markedly raise the pain thresholds and relieve inflammatory pain. SGE could attenuate the pathological damage, inhibit P2X3 expression, inhibit the elevation of inflammatory factors caused by α, β me-ATP. SGE can also inhibit NF-κB and ERK1/2 activation caused by α, β me-ATP, and inhibit the mRNA expression of P2X3, COX-2, NF-κB, IL-1β, IL-6 and TNF-α in DRG of rats induced by CFA coupled with α, β me-ATP. Conclusions: In summary, our research indicated that SGE could alleviate CFA-induced inflammatory pain by suppression of P2X3 receptor.