Department of Rehabilitation in Traditional Chinese Medicine, The Second Affiliated Hospital of Zhejiang University School of Medicine, No. 88, Jiefang Road, Hangzhou City, Zhejiang Province 310009, China; Department of Acupuncture and Rehabilitation, Affiliated Hospital of Nanjing University of Chinese Medicine, Jiangsu Province Hospital of Chinese Medicine, 155 Hanzhong Road, Nanjing City, Jiangsu 210029, China.
The Third Affiliated Hospital of Zhejiang Chinese Medical University, 219 Moganshan Road, Xihu District, Hangzhou City, Zhejiang Province 310005, China.
Neurosci Lett. 2024 Jan 18;820:137611. doi: 10.1016/j.neulet.2023.137611. Epub 2023 Dec 22.
Chronic pain is acomplexhealth issue. Compared to acute pain, which has a protective value, chronic pain is defined as persistent pain after tissue injury. Few clinical advances have been made to prevent the transition from acute to chronic pain. Electroacupuncture (EA), the most common form of acupuncture, is widely used in clinical practice to relieve pain.
The hyperalgesic priming model, established via a carrageenan injection followed by a prostaglandin E injection, was used to investigate the development or establishment of chronic pain. We observed the hyperalgesic effect of EA on rats and investigated the expression p38 mitogen-activated protein kinase, interleukin-33 (IL-33), and its receptor ST2 in astrocytes in the L4-L6 spinal cord dorsal horns (SDHs) after EA. The IL-33/ST2 signaling pathway in SDH is associated with the development of chronic pain.
EA can reverse the pain threshold in hyperalgesic priming model rats and regulates the expression of phosphorylated p38, IL-33, and ST2 in astrocytes in the L4-L6 SDHs. We discovered that EA raises the pain threshold. This suggests that EA can prevent the development or establishment of chronic pain by inhibiting IL-33/ST2 signaling in the lower central nervous system.
EA can alleviate the development or establishment of chronic pain by modulating IL-33/ST2 signaling in SDHs. Our findings will help clinicians understand the mechanisms of EA analgesia.
慢性疼痛是一种复杂的健康问题。与具有保护价值的急性疼痛不同，慢性疼痛被定义为组织损伤后的持续疼痛。很少有临床进展可以预防急性疼痛向慢性疼痛的转变。电针（EA）是最常见的针灸形式，广泛应用于临床实践中以缓解疼痛。
我们使用角叉菜胶注射后再注射前列腺素 E 的方法建立痛觉过敏启动模型，以研究慢性疼痛的发展或建立。我们观察了 EA 对大鼠的痛觉过敏效应，并研究了 EA 后 L4-L6 脊髓背角（SDH）星形胶质细胞中 p38 丝裂原活化蛋白激酶、白细胞介素 33（IL-33）及其受体 ST2 的表达。SDH 中的 IL-33/ST2 信号通路与慢性疼痛的发展有关。
EA 可以逆转痛觉过敏启动模型大鼠的痛觉阈值，并调节 L4-L6 SDH 中星形胶质细胞中磷酸化 p38、IL-33 和 ST2 的表达。我们发现 EA 提高了痛觉阈值。这表明 EA 通过抑制中低级中枢神经系统中的 IL-33/ST2 信号，可预防慢性疼痛的发展或建立。
EA 通过调节 SDH 中的 IL-33/ST2 信号，可以缓解慢性疼痛的发展或建立。我们的发现将帮助临床医生了解 EA 镇痛的机制。
