中华医学杂志（英文版）
中華醫學雜誌（英文版）
중화의학잡지（영문판）
Chinese Medical Journal
2015年
17期
2340-2345
,共6页
c-Jun%c-Jun NH2-terminal Kinase%L5 Spinal Nerve Ligation%Najanalgesin
Background:Najanalgesin,a toxin isolated from the venom ofNaja naja atra,has been shown to exert significant analgesic effects in a neuropathic pain model in rats.However,the molecular mechanism underlying this protective effect of najanalgesin is poorly understood.The present study sought to evaluate the intracellular signaling pathways that are involved in the antinociceptive effect of najanalgesin on neuropathic pain.Methods:The antinociceptive properties of najanalgesin were tested in hind paw withdrawal thresholds in response to mechanical stimulation.We analyzed the participation of the mitogen-activated protein kinase p38,extracellular-regulated kinase (ERK),and c-Jun N-terminal kinase (JNK) by western blot analysis.This inhibition of JNK was confirmed by immunohistochemistry.Results:The phosphorylation levels of JNK (as well as its downstream molecule c-Jun),p38,and ERK were significantly increased after injury.Najanalgesin only inhibited JNK and c-Jun phosphorylation but had no effect on either ERK or p38.This inhibition of JNK was confirmed by immunohistochemistry,which suggested that the antinociceptive effect of najanalgesin on spinal nerve ligation-induced neuropathic pain in rats is associated with JNK activation in the spinal cord.Conclusion:The antinociceptive effect of naj analgesin functions by inhibiting the JNK in a neuropathic pain model.
