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电针通过脊髓阿片能和肾上腺素能机制对小鼠紫杉醇诱导的神经性疼痛的镇痛作用

Analgesic effect of electroacupuncture on paclitaxel-induced neuropathic pain via spinal opioidergic and adrenergic mechanisms in mice.

作者信息

Choi Jung-Wan, Kang Suk-Yun, Choi Jae-Gyun, Kang Dong-Wook, Kim Soo-Jin, Lee Sang Do, Park Jin Bong, Ryu Yeon-Hee, Kim Hyun-Woo

机构信息

Department of Physiology and Brain Research Institute, Chungnam National University, School of Medicine, Daejeon 301-747, South Korea.

出版信息

Am J Chin Med. 2015;43(1):57-70. doi: 10.1142/S0192415X15500044. Epub 2015 Feb 2.

DOI:10.1142/S0192415X15500044
PMID:25640847
Abstract

This study was designed to determine the antinociceptive effect and related neuronal mechanism of electroacupuncture (EA) on paclitaxel (PTX)-induced neuropathic pain in mice. PTX (4 mg/kg, i.p.) was administered once a day for 5 consecutive days to induce neuropathic pain. EA stimulation (2 mA, 2 Hz, 30 min) was applied at the ST36 acupoint bilaterally once in every 2 days. Repeated EA stimulation significantly attenuated PTX-induced mechanical allodynia and thermal hyperalgesia. In a separate set of experiment, the antinociceptive effect of a single EA stimulation 8 days after PTX treatment was reduced by intrathecal pretreatment with naloxone (opioid receptor antagonist), idazoxan (alpha2-adrenoceptor antagonist) or propranolol (beta-adrenoceptor antagonist), but not prazosin (alpha1-adrenoceptor antagonist). Moreover, EA remarkably suppressed the PTX-enhanced phosphorylation of the NMDA receptor NR2B subunit in the spinal dorsal horn, and intrathecal pretreatment of naloxone, idazoxan (IDA) or propranolol blocked the effect of EA. In conclusion, EA stimulation at the ST36 acupoint significantly diminished PTX-induced neuropathic pain in mice via the mediation of spinal opioid receptor, alpha2- and beta-adrenoceptors.

摘要

本研究旨在确定电针(EA)对紫杉醇(PTX)诱导的小鼠神经性疼痛的镇痛作用及相关神经机制。连续5天每天腹腔注射PTX(4 mg/kg)以诱导神经性疼痛。每隔2天在双侧足三里穴进行一次EA刺激(2 mA,2 Hz,30分钟)。重复EA刺激可显著减轻PTX诱导的机械性异常性疼痛和热痛觉过敏。在另一组实验中,PTX治疗8天后单次EA刺激的镇痛作用被鞘内注射纳洛酮(阿片受体拮抗剂)、咪唑克生(α2肾上腺素能受体拮抗剂)或普萘洛尔(β肾上腺素能受体拮抗剂)减弱,但哌唑嗪(α1肾上腺素能受体拮抗剂)无此作用。此外,EA显著抑制了脊髓背角中PTX增强的NMDA受体NR2B亚基的磷酸化,鞘内注射纳洛酮、咪唑克生(IDA)或普萘洛尔可阻断EA的作用。总之,针刺足三里穴通过脊髓阿片受体、α2和β肾上腺素能受体介导,显著减轻PTX诱导的小鼠神经性疼痛。

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