Downregulation of Spinal G Protein-Coupled Kinase 2 Abolished the Antiallodynic Effect of Electroacupuncture.
Downregulation of Spinal G Protein-Coupled Kinase 2 Abolished the Antiallodynic Effect of Electroacupuncture.
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脊髓 G 蛋白偶联激酶 2 的下调消除了电针的抗异常疼痛作用
DOI：
10.1155/2015/848603
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发表时间：
2015
期刊：
影响因子：
--
通讯作者：
Mao-Ying QL
中科院分区：
文献类型：
--
作者：
Liu H;Liu SB;Li Q;Wang H;Wang YQ;Mao-Ying QL
针灸或电针（EA）已被证明对炎症性疼痛具有强大的抗hypernociceptive作用。G蛋白偶联受体激酶2（GRK2）在脊髓和外周伤害性感受器中的衰减被广泛认为是促进急性疼痛向慢性疼痛的转变和促进伤害性感受的进展。本研究旨在探讨脊髓GRK 2在电针抗完全弗氏佐剂（CFA）诱导的炎症痛大鼠模型中的可能作用。注射CFA后第1天电针足三里穴和昆仑穴。在CFA注射后第1天单次电针治疗显著减轻了电针后2小时CFA引起的机械性异常性疼痛。重复电针从第2次开始显示出明显的抗异常性疼痛作用，在其余的治疗中观察到持续的效果。然而，脊髓GRK2的下调，鞘内暴露GRK2反义30分钟后，电针治疗完全消除了短暂的和持久的抗异常性疼痛的效果。这些数据表明脊髓GRK2在电针抗炎性痛的异常性疼痛中起重要作用。
Acupuncture or electroacupuncture (EA) has been demonstrated to have a powerful antihypernociceptive effect on inflammatory pain. The attenuation of G protein-coupled receptor kinase 2 (GRK2) in spinal cord and peripheral nociceptor has been widely acknowledged to promote the transition from acute to chronic pain and to facilitate the nociceptive progress. This study was designed to investigate the possible role of spinal GRK2 in EA antiallodynic in a rat model with complete Freund's adjuvant (CFA) induced inflammatory pain. EA was applied to ST36 (“Zusanli”) and BL60 (“Kunlun”) one day after CFA injection. Single EA treatment at day 1 after CFA injection remarkably alleviated CFA induced mechanical allodynia two hours after EA. Repeated EA displayed significant antiallodynic effect from 2nd EA treatment and a persistent effect was observed during the rest of treatments. However, downregulation of spinal GRK2 by intrathecal exposure of GRK2 antisense 30 mins after EA treatment completely eliminated both the transient and persistent antiallodynic effect by EA treatment. These pieces of data demonstrated that the spinal GRK2 played an important role in EA antiallodynia on inflammatory pain.
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影响因子：
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