关键词: 受体相互作用蛋白激酶3, 神经病理性疼痛, 腰5脊神经结扎模型

Abstract:

Objective To observe the expression of receptor- mediated protein kinase 3 （RIP3） in a rat model of spinal nerve ligation and explore whether it is involved in the pathogenesis of neuropathic pain. Methods Rats were randomly divided into four groups： operation，saline，inhibitor and sham operation（n=10 rats per group）. In the operation，saline，and inhibitor groups，a lumbar 5 spinal nerve ligation model was established. Animals in the sham operation group underwent surgery without nerve ligation. In the inhibitor group，GSK'872 was injected intrathecally at 30 min before model establishment；in the saline group，the same volume of saline was intrathecally injected. Behavior and mechanical allodynia were recorded for each group. RIP3 expression was analyzed using immuno- histochemistry and Western blotting；TNF-α and IL-1β levels were determined using ELISA. Results The operation and saline groups showed significant behavioral differences，significantly lower mechanical allodynia，as well as significantly higher levels of RIP3 protein，TNF-α and IL-1β than the sham operation group（P＜0.05）. The inhibitor group showed lower mechanical pain sensitivity and protein content than the operation and saline groups （P＜0.05）. Expression of RIP3，TNF-α and IL-1β negatively correlated with mechanical allodynia. Conclusions RIP3 is up-regulated in this animal model of neuropathic pain，so RIP3 may be involved in the development of neuropathic pain.

Key words: Receptor-interacting protein kinase 3, Neuropathic pain, Lumbar 5 Spinal nerve ligation model