Silencing of Id2 Alleviates Chronic Neuropathic Pain Following Chronic Constriction Injury

被引:1
作者
Jiang, Liuming [1 ]
Wu, Qun [1 ]
Yang, Tao [1 ]
机构
[1] Wenzhou Med Univ, Affiliated Hosp 1, Dept Anesthesiol, 2 Fuxue Rd, Wenzhou 325000, Zhejiang, Peoples R China
关键词
Inhibitor of DNA binding/differentiation 2 (Id2); Neuropathic pain; Chronic constriction injury (CCI); NF-kappa B; PERIPHERAL-NERVE INJURY; NECROSIS-FACTOR-ALPHA; RAT SCIATIC-NERVE; KAPPA-B PATHWAY; UP-REGULATION; HYPERALGESIA; EXPRESSION; HYPERSENSITIVITY; CONTRIBUTES; ALLODYNIA;
D O I
10.1007/s12031-016-0713-z
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Inhibitor of DNA binding/differentiation 2 (Id2) belongs to a helix-loop-helix family of proteins. Recent studies have showed that Id2 plays a pivotal role in neuronal survival and neuroprotection. However, under neuropathic pain conditions, the role of Id2 is still unclear. In this study, we investigated the effect of Id2 on neuropathic pain in a rat chronic constriction injury (CCI) model. Our results demonstrated that Id2 was upregulated in the dorsal root ganglion (DRG) in a CCI rat in a time-dependent manner. Intrathecal short-hairpin RNA (shRNA)-Id2 attenuates mechanical allodynia and thermal hyperalgesia in CCI rats, and inhibits the expression of TNF-alpha and IL-1 beta in the DRG in CCI rats. Furthermore, knockdown of Id2 reduces the expression of NF-kappa B p65 in the DRG of CCI rats. Taken together, our findings suggest that knockdown of Id2 may alleviate neuropathic pain by inhibiting the NF-kappa B activation to inhibit the production of pro-inflammatory mediators. Therefore, Id2 may provide an important target of neuropathic pain treatment.
引用
收藏
页码:99 / 105
页数:7
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