Ke Zhongling, Huang Yuxian, Wang Ang, Chen Yanhui
Fujian Medical University Union Hospital, Fuzhou, 350001, China.
J Neuroimmune Pharmacol. 2025 May 20;20(1):56. doi: 10.1007/s11481-025-10214-5.
Neuroinflammation plays a vital role in the etiology and pathogenesis of Tourette syndrome (TS). The postmortem report of TS patients clarified that IL-2 is elevated in the basal ganglia region, supporting neuroinflammation of TS. α receptor agonist (clonidine) is one of the primary drugs for treating tic disorders; supported by clinical and animal experiments, α receptor agonists have potential anti-inflammatory effects. This article aims to explore the impact of clonidine on neuroinflammation with TS and to reveal the possible mechanism of clonidine-mediated neuroinflammation with TS. Thirty P21 SD rats were randomly divided into a TS rat group (n = 20) and a normal control group (n = 10). After successful TS modelling, rats were randomly divided into the clonidine intervention group (n = 10) and the TS group (n = 10). The clonidine intervention group received clonidine 0.1 mg/kg by gavage daily for seven consecutive days. After behavioural evaluation on day 8, the brain was removed from the head. The striatum was separated from one side of the brain and subjected to ELISA to detect cytokines. The other side of the brain was subjected to immunohistochemical detection for microglial activation, and the integral optical density value was calculated using image software for comparison between the groups. Compared to the normal group, IL-2 cytokine levels in TS rats were significantly higher (P < 0.05). In the clonidine group, IL-2 levels (213.82 ± 121.48 pg/ml) were significantly lower than in the TS group (322.61 ± 79.27 pg/ml) (P < 0.05) but not significantly different from the normal control group (257.40 ± 95.80 pg/ml) (P > 0.05). Immunohistochemical analysis showed significant microglial activation in TS rats (IOD = 22.10 ± 6.67) compared to the normal group (IOD = 11.58 ± 4.36) (P < 0.05). Clonidine administration reduced microglial activation, with a significant difference between the TS + clonidine group (IOD = 15.97 ± 8.03) and TS rats (P < 0.05). Clonidine can suppress the neuroinflammatory response in Tourette syndrome, and its inhibitory effect on the neuroinflammatory response may be a potential beneficial effect of this treatment.
神经炎症在抽动秽语综合征（TS）的病因和发病机制中起着至关重要的作用。TS患者的尸检报告表明，基底神经节区域的白细胞介素-2（IL-2）水平升高，支持了TS的神经炎症。α受体激动剂（可乐定）是治疗抽动障碍的主要药物之一；临床和动物实验表明，α受体激动剂具有潜在的抗炎作用。本文旨在探讨可乐定对TS神经炎症的影响，并揭示可乐定介导TS神经炎症的可能机制。将30只P21 SD大鼠随机分为TS大鼠组（n = 20）和正常对照组（n = 10）。成功建立TS模型后，将大鼠随机分为可乐定干预组（n = 10）和TS组（n = 10）。可乐定干预组连续7天每天经口灌胃给予0.1 mg/kg可乐定。在第8天进行行为评估后，将大鼠断头取脑。从一侧脑部分离出纹状体，采用酶联免疫吸附测定法（ELISA）检测细胞因子。另一侧脑进行免疫组织化学检测小胶质细胞活化情况，使用图像软件计算积分光密度值，用于组间比较。与正常组相比，TS大鼠的IL-2细胞因子水平显著升高（P < 0.05）。在可乐定组中，IL-2水平（213.82±121.48 pg/ml）显著低于TS组（322.61±79.27 pg/ml）（P < 0.05），但与正常对照组（257.40±95.80 pg/ml）无显著差异（P > 0.05）。免疫组织化学分析显示，与正常组（积分光密度值[IOD] = 11.58±4.36）相比，TS大鼠存在显著的小胶质细胞活化（IOD = 22.10±6.67）（P < 0.05）。给予可乐定可降低小胶质细胞活化，TS + 可乐定组（IOD = 15.97±8.03）与TS大鼠之间存在显著差异（P < 0.05）。可乐定可抑制抽动秽语综合征中的神经炎症反应，其对神经炎症反应的抑制作用可能是该治疗的潜在有益效果。
