Li Sisi, Jiang Xia, Wu Qiaoyun, Jin Yun, He Rong, Hu Jie, Zheng Yuyin
Department of Physical Medicine and Rehabilitation, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, China.
Integrative & Optimized Medicine Research Center, China-USA Institute for Acupuncture and Rehabilitation of Wenzhou Medical University, Wenzhou, Zhejiang, China.
Evid Based Complement Alternat Med. 2022 Oct 7;2022:4505934. doi: 10.1155/2022/4505934. eCollection 2022.
Neuropathic pain remains a chronic and intractable pain. Recent studies have shown a close relationship between gamma-aminobutyric acid A (GABAA) receptor and neuropathic pain. Spinal cord GABAA receptors are key modulators of pain processing. Electroacupuncture (EA) is currently used worldwide to relieve pain. The immunomodulatory effect of EA in animals has been proposed in previous studies. However, it remains unclear how EA contributes to alleviating neuropathic pain. In this study, the chronic constriction injury (CCI) rat model was used to explore the relationship between GABAA receptor and neuropathic pain. We also investigated whether EA treatment could ameliorate pain hypersensitivity by modulating the GABAA receptor. To determine the function of EA in neurological diseases, in this study, the mechanical withdrawal threshold (MWT) and thermal withdrawal latency (TWL) were assessed to determine the threshold of pain. In addition, we used Western blot, immunofluorescence, and real-time quantitative PCR to confirm whether EA treatment relieves pain hypersensitivity by regulating GABAA receptors. The morphology of synapse was examined using an electron microscope. In the present study, EA relieved mechanical allodynia and thermal hyperalgesia. EA also inhibited microglial activation in the spinal cord, accompanied by increased levels of GABAAR2, GABAAR3, and GABAAR2 subunits. However, the analgesic effect of EA was attenuated by treatment with the GABAA receptor antagonist bicuculine. Overall, the present results indicate that microglia and GABAA receptor might participate in EA analgesia. These results contribute to our understanding of the impact of EA on rats after sciatic nerve compression, providing a theoretical basis for the clinical application of EA analgesia.
神经病理性疼痛仍然是一种慢性难治性疼痛。最近的研究表明，γ-氨基丁酸A（GABAA）受体与神经病理性疼痛之间存在密切关系。脊髓GABAA受体是疼痛处理的关键调节因子。电针（EA）目前在全球范围内用于缓解疼痛。先前的研究提出了EA在动物中的免疫调节作用。然而，EA如何减轻神经病理性疼痛仍不清楚。在本研究中，采用慢性缩窄损伤（CCI）大鼠模型来探讨GABAA受体与神经病理性疼痛之间的关系。我们还研究了EA治疗是否可以通过调节GABAA受体来改善疼痛超敏反应。为了确定EA在神经疾病中的作用，在本研究中，评估了机械撤针阈值（MWT）和热撤针潜伏期（TWL）以确定疼痛阈值。此外，我们使用蛋白质免疫印迹法、免疫荧光法和实时定量PCR来确认EA治疗是否通过调节GABAA受体来减轻疼痛超敏反应。使用电子显微镜检查突触的形态。在本研究中，EA减轻了机械性异常性疼痛和热痛觉过敏。EA还抑制了脊髓中的小胶质细胞活化，同时伴有GABAAR2、GABAAR3和GABAAR2亚基水平的升高。然而，GABAA受体拮抗剂荷包牡丹碱的治疗减弱了EA的镇痛作用。总体而言，目前的结果表明小胶质细胞和GABAA受体可能参与了EA镇痛。这些结果有助于我们理解EA对坐骨神经压迫后大鼠的影响，为EA镇痛的临床应用提供理论依据。
