Huang Tao, Fu Bo, Wang Jing, Wang Bin, Liu Shao-Jun, Weng Xie-Chuan
Department of Biology, Institute of Basic Medical Science, Academy of Military Medical Science.
State Key Laboratory of Proteomics, Beijing 100850.
Zhongguo Ying Yong Sheng Li Xue Za Zhi. 2017 Apr 8;33(4):294-298. doi: 10.12047/j.cjap.5574.2017.072.
To explore the effects of hyperpolarization-activated cyclic nucleotide-gated channels 2(HCN2) in the formation of peripheral neuropathic pain in rats.
Twenty-four healthy adult rats were divided into two groups randomly(=12):the sham group rats were only isolated the left L4, L5 spinal nerve, the spinal nerve ligation(SNL) group was separated the spinal nerve and performed the corresponding ligation. The behavioral experiments were tested 7 days after operation; The model rats were randomly divided into 3 groups(=6):① negative group(Saline), intra-plantar injection of saline in left hindpaws; ② positive group(gabapentin, GBPT), intraperitoneal injection of gabapentin; ③ experimental group(ZD7288), intra-plantar injection of ZD7288 in left hindpaws. The behavioral experiments were tested before injection and 1 h, 4 h, 24 h and 48 h after injection; Obtaining the dorsal root ganglion(DRG) of the control group (before operation), sham group and the SNL group(=6), using qPCR and Western blot to analyze the mRNA and protein of HCN2 in rats' DRG.
The rat model of neuropathic pain was successfully established. Compared with saline group, GBPT group and ZD7288 group could significantly reduce the symptoms of neuropathic pain in rats after injection 1 h (<0.01), and there was no difference between GBPT group and ZD7288 group. Compared with control group and sham group, the expression of HCN2 mRNA in SNL group's DRG was significantly increased (<0.01), and the expression of HCN2 channel protein was also increased significantly (<0.05).
HCN2 is involved in the development of peripheral neuropathic pain and is likely to be a potential new target for the treatment of neuropathic pain.
探讨超极化激活环核苷酸门控通道2（HCN2）在大鼠周围神经病理性疼痛形成中的作用。
将24只健康成年大鼠随机分为两组（每组12只）：假手术组大鼠仅分离左侧L4、L5脊神经，脊神经结扎（SNL）组分离脊神经并进行相应结扎。术后7天进行行为学实验；将模型大鼠随机分为3组（每组6只）：①阴性组（生理盐水组），左后足跖内注射生理盐水；②阳性组（加巴喷丁组，GBPT），腹腔注射加巴喷丁；③实验组（ZD7288组），左后足跖内注射ZD7288。在注射前及注射后1小时、4小时、24小时和48小时进行行为学实验；获取对照组（术前）、假手术组和SNL组（每组6只）的背根神经节（DRG），采用qPCR和蛋白质免疫印迹法分析大鼠DRG中HCN2的mRNA和蛋白表达。
成功建立神经病理性疼痛大鼠模型。与生理盐水组相比，GBPT组和ZD7288组在注射后1小时可显著减轻大鼠神经病理性疼痛症状（P<0.01），GBPT组和ZD7288组之间无差异。与对照组和假手术组相比，SNL组DRG中HCN2 mRNA表达显著增加（P<0.01），HCN2通道蛋白表达也显著增加（P<0.05）。
HCN2参与周围神经病理性疼痛的发生发展，可能是治疗神经病理性疼痛的潜在新靶点。
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