Department of Neurobiology, School of Basic Medicine, Tongji Medical College of Huazhong University of Science and Technology, China.
Department of Acupuncture & Moxibustion, Wuhan Hospital of Integrated Chinese & Western Medicine, Tongji Medical College of Huazhong University of Science and Technology, China.
Biomed Res Int. 2021 Mar 8;2021:6637693. doi: 10.1155/2021/6637693. eCollection 2021.
Postherpetic neuralgia (PHN) is a complication of herpes zoster viral infection. Its main manifestations are continuous or intermittent burning-like and electroshock-like pain in the affected nerves. Electroacupuncture (EA) is widely used in clinical treatment and exerts effects in alleviating neuropathic pain. In this study, we investigated the effect and underlying mechanism of EA on PHN. Sprague-Dawley rats were treated with resiniferatoxin (RTX) to establish a PHN model and subjected to EA and/or miR-223-3p overexpression (OV) or interference. Mechanical withdrawal latency was measured as an indication of pain sensitivity. Hematoxylin-eosin staining and transmission electron microscopy were performed to observe neuron cell morphology and autophagic vacuoles, respectively. ELISA was performed to detect reactive oxygen species (ROS) production and the levels of tumor necrosis factor- (TNF-) , inducible nitric oxide synthase (iNOS), interleukin- (IL-) 6, and IL-10. Changes in autophagy and apoptosis-related miRNAs were detected by immunofluorescence and qRT-PCR, respectively. In RTX-treated rats, OV and EA reduced pain sensitivity, decreased the number of eosinophils, and increased that of nerve cells. ROS generation and the levels of TNF- and iNOS were significantly reduced, while those of IL-6 and IL-10 were increased. OV and EA induced fewer autophagic vacuoles than those in the model group. The expression of autophagy-related protein microtubule-associated protein 1 light chain 3-II, ATG9, and Rab1 was decreased by OV and EA, whereas that of P62 was increased. qRT-PCR revealed that miR-223-3p expression in the model group decreased but was increased by EA. EA inhibits neuron cell autophagy in PHN by increasing miR-223-3p expression.
带状疱疹后神经痛 (PHN) 是带状疱疹病毒感染的并发症。其主要表现为受累神经的持续性或间歇性灼烧样和电击样疼痛。电针 (EA) 广泛应用于临床治疗，对缓解神经病理性疼痛具有疗效。在本研究中，我们探讨了 EA 对 PHN 的作用及其潜在机制。用树脂毒素 (RTX) 处理 Sprague-Dawley 大鼠以建立 PHN 模型，并进行 EA 和/或 miR-223-3p 过表达 (OV) 或干扰。通过测量机械退缩潜伏期来评估疼痛敏感性。通过苏木精-伊红染色和透射电子显微镜观察神经元细胞形态和自噬空泡，分别。通过 ELISA 检测活性氧 (ROS) 产生以及肿瘤坏死因子- (TNF-) 、诱导型一氧化氮合酶 (iNOS)、白细胞介素- (IL-) 6 和 IL-10 的水平。通过免疫荧光和 qRT-PCR 分别检测自噬和凋亡相关 miRNAs 的变化。在 RTX 处理的大鼠中，OV 和 EA 降低了疼痛敏感性，减少了嗜酸性粒细胞的数量，增加了神经细胞的数量。ROS 的生成以及 TNF-和 iNOS 的水平明显降低，而 IL-6 和 IL-10 的水平升高。OV 和 EA 诱导的自噬空泡少于模型组。OV 和 EA 降低了自噬相关蛋白微管相关蛋白 1 轻链 3-II、ATG9 和 Rab1 的表达，增加了 P62 的表达。qRT-PCR 显示模型组中 miR-223-3p 的表达降低，但 EA 组表达增加。EA 通过增加 miR-223-3p 的表达抑制 PHN 中的神经元细胞自噬。
