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右美托咪定对奥沙利铂诱导的大鼠神经性疼痛的镇痛作用

[Analgesic effect of dexmedetomidine on oxaliplatin-induced neuropathic pain in rats].

作者信息

Li Shuangfeng, Ouyang Bishan, Zhao Xin, Wang Yaping

机构信息

Department of Anesthesiology, Second Xiangya Hospital of Central South University, Changsha 410011, China.

Department of Anesthesiology, Hainan General Hospital, Haikou 570311, China.

出版信息

Nan Fang Yi Ke Da Xue Xue Bao. 2018 Jul 30;38(7):836-841. doi: 10.3969/j.issn.1673-4254.2018.07.11.

Abstract

OBJECTIVE

To investigate the analgesic effect of dexmedetomidine (Dex) on oxaliplatin-induced neuropathic pain in rats and explore its mechanism.

METHODS

SD rats were randomly divided into control, model, Dextreatment, and Dex + atipamezole groups. In the latter 3 groups, rat models of neuropathic pain were established by a single intraperitoneal injection of oxaliplatin. The paw withdrawal threshold (PWT) to mechanical stimuli and tail withdrawal latency (TWL) to thermal stimuli of the rats were determined. Western blotting and immunofluorescence assay were performed to observe the expression of spinal phosphorylated STAT3 (p-STAT3) in the rats.

RESULTS

Compared with the rats in the control group, the rats in the model group and Dex+atipamezole group showed significantly decreased PWT and TWL (cold) and increased expression of p-STAT3 in the spinal cord ( < 0.05). In Dex group, PWT and TWL (cold) were significantly increased ( < 0.05) and p-STAT3 expression in the spinal cord was significantly decreased ( < 0.01) 60 to 120 after Dex treatment as compared with those in the model group, and these effects of Dex were significantly attenuated by the administration of atipamezole ( < 0.05).

CONCLUSIONS

Dex can alleviate oxaliplatin-induced neuropathic pain in rats by inhibiting the phosphorylation of STAT3 in the spinal cord.

摘要

目的

探讨右美托咪定(Dex)对奥沙利铂诱导的大鼠神经性疼痛的镇痛作用并探究其机制。

方法

将SD大鼠随机分为对照组、模型组、Dex治疗组和Dex+阿替美唑组。后3组通过单次腹腔注射奥沙利铂建立神经性疼痛大鼠模型。测定大鼠对机械刺激的爪部缩足阈值(PWT)和对热刺激的尾部缩尾潜伏期(TWL)。采用蛋白质免疫印迹法和免疫荧光法观察大鼠脊髓中磷酸化信号转导和转录激活因子3(p-STAT3)的表达。

结果

与对照组大鼠相比,模型组和Dex+阿替美唑组大鼠的PWT和TWL(冷刺激)显著降低,脊髓中p-STAT3表达增加(P<0.05)。与模型组相比,Dex组在Dex治疗60至120分钟后PWT和TWL(冷刺激)显著增加(P<0.05),脊髓中p-STAT3表达显著降低(P<0.01),且阿替美唑给药可显著减弱Dex的这些作用(P<0.05)。

结论

Dex可通过抑制脊髓中STAT3的磷酸化减轻奥沙利铂诱导的大鼠神经性疼痛。

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