Fang Junfan, Wang Sisi, Zhou Jie, Shao Xiaomei, Sun Haiju, Liang Yi, He Xiaofen, Jiang Yongliang, Liu Boyi, Jin Xiaoming, Fang Jianqiao, Du Junying
Department of Neurobiology and Acupuncture Research, The Third Clinical Medical College, Zhejiang Chinese Medical University, Key Laboratory of Acupuncture and Neurology of Zhejiang Province, Hangzhou, China.
Department of Anatomy, Cell Biology and Physiology, Stark Neuroscience Research Institute, Indiana University School of Medicine, Indianapolis, IN, United States.
Front Neurosci. 2021 Jul 20;15:685715. doi: 10.3389/fnins.2021.685715. eCollection 2021.
Many cases of acute pain can be resolved with few side effects. However, some cases of acute pain may persist beyond the time required for tissue injury recovery and transit to chronic pain, which is hard to treat. The mechanisms underlying pain transition are not entirely understood, and treatment strategies are lacking. In this study, the hyperalgesic priming model was established on rats to study pain transition by injection of carrageenan (Car) and prostaglandin E2 (PGE2). The expression levels of protein kinase C epsilon (PKCε) and transient receptor potential vanilloid 1 (TRPV1) in the L4-L6 dorsal root ganglion (DRG) were investigated. Electroacupuncture (EA) is a form of acupuncture in which a small electric current is passed between a pair of acupuncture needles. EA was administrated, and its effect on hyperalgesia and PKCε and TRPV1 expression was investigated. The PKCε-TRPV1 signaling pathway in DRG was implicated in the pain transition. EA increased the pain threshold of model animals and regulated the high expression of PKCε and TRPV1. Moreover, EA also regulated hyperalgesia and high TRPV1 expression induced by selective PKCε activation. We also found that EA partly increased chronic pain threshold, even though it was only administered between the Car and PGE2 injections. These findings suggested that EA could prevent the transition from acute to chronic pain by inhibiting the PKCε and TRPV1 expression in the peripheral nervous system.
许多急性疼痛病例可以在副作用较少的情况下得到缓解。然而,一些急性疼痛病例可能会持续超过组织损伤恢复所需的时间,并转变为难以治疗的慢性疼痛。疼痛转变的潜在机制尚未完全明确,且缺乏相应的治疗策略。在本研究中,通过给大鼠注射角叉菜胶(Car)和前列腺素E2(PGE2)建立痛觉过敏预激发模型,以研究疼痛转变。研究了L4-L6背根神经节(DRG)中蛋白激酶Cε(PKCε)和瞬时受体电位香草酸亚型1(TRPV1)的表达水平。电针(EA)是一种针灸形式,在一对针灸针之间通过小电流。实施电针治疗,并研究其对痛觉过敏以及PKCε和TRPV1表达的影响。DRG中的PKCε-TRPV1信号通路与疼痛转变有关。电针提高了模型动物的痛阈,并调节了PKCε和TRPV1的高表达。此外,电针还调节了由选择性PKCε激活诱导的痛觉过敏和TRPV1高表达。我们还发现,即使电针仅在注射Car和PGE2之间实施,它也部分提高了慢性疼痛阈值。这些发现表明,电针可通过抑制外周神经系统中PKCε和TRPV1的表达来预防急性疼痛向慢性疼痛的转变。