Kamal Mennat-Allah M, Essam Reham M, Abdelkader Noha F, Zaki Hala F
Central Health Laboratories, Ministry of Health, Cairo, Egypt.
Department of Pharmacology, Faculty of Pharmacy, Cairo University, Cairo, Egypt.
J Neuroimmune Pharmacol. 2025 Apr 15;20(1):38. doi: 10.1007/s11481-025-10194-6.
Fibromyalgia syndrome (FMS) is characterized by prolonged, widespread musculoskeletal pain accompanied by various physical and psychological disturbances. Modafinil, a wake-promoting drug, manages pain symptoms in several diseases by inhibiting dopamine reuptake and exhibiting anti-inflammatory and immunomodulatory effects, including the impairment of cytokine production, microglia, and mast cell activation. Central inflammation may involve microglial activation, which is correlated with mast cell activation. Restoring dopamine levels and modulating the communication between mast cells and microglia may represent a promising approach to managing pain symptoms in FMS. Thus, this study intended to explore the interplay between brain mast cells and microglia as an underlying mechanism in the pathophysiology of FMS and how this interaction is controlled by modafinil, with a focus on dopamine/SP/MRGPRX2/histamine and PI3K/p-Akt/NF-κB signaling pathways. Rats were arbitrarily distributed between 4 groups. Group 1 served as normal control. Reserpine (1 mg/kg/day; s.c) was injected into the remaining groups for three consecutive days. In groups 3 and 4, modafinil (100 mg/kg/day; p.o) was administered either alone or in conjunction with haloperidol (1 mg/kg/day; ip), respectively, for the following 21 days. Modafinil ameliorated reserpine-induced thermal/mechanical allodynia (1.3-fold, 2.3-fold) and hyperalgesia (0.5-fold), attenuated depression (0.5-fold), and enhanced motor coordination (1.2-fold). It mitigated the histopathological alterations and increased dopamine levels in the thalamus of rats by 88.5%. Modafinil displayed anti-inflammatory effects via inhibiting mast cells and microglia activation, manifested by reductions in SP/MRGPRX2/IL-17/histamine (52%, 58%, 56.7%, and 63.7%) and PI3K/p-Akt/t-Akt/NF-κB/TNF-α/IL-6 (31.7%, 55.5%, 41%, 47.6%, and 76.9%), respectively. Ultimately, modafinil alleviated FMS behavioral, histopathological, and biochemical abnormalities and suppressed mast cell-microglial neuroinflammation in the thalamus of rats exposed to reserpine. This study highlights the potential of repurposing modafinil to improve FMS symptoms.
纤维肌痛综合征(FMS)的特征是长期广泛的肌肉骨骼疼痛,并伴有各种身体和心理障碍。莫达非尼是一种促醒药物,通过抑制多巴胺再摄取以及发挥抗炎和免疫调节作用(包括抑制细胞因子产生、小胶质细胞和肥大细胞活化)来控制多种疾病的疼痛症状。中枢炎症可能涉及小胶质细胞活化,这与肥大细胞活化相关。恢复多巴胺水平并调节肥大细胞与小胶质细胞之间的通讯可能是控制FMS疼痛症状的一种有前景的方法。因此,本研究旨在探讨脑内肥大细胞与小胶质细胞之间的相互作用,作为FMS病理生理学的潜在机制,以及这种相互作用如何受莫达非尼调控,重点关注多巴胺/速激肽/ MRGPRX2 /组胺和PI3K / p-Akt / NF-κB信号通路。将大鼠随机分为4组。第1组作为正常对照组。连续三天给其余组皮下注射利血平(1mg/kg/天)。在第3组和第4组中,在接下来的21天里,分别单独给予莫达非尼(100mg/kg/天;口服)或与氟哌啶醇(1mg/kg/天;腹腔注射)联合给药。莫达非尼改善了利血平诱导的热/机械性痛觉过敏(1.3倍、2.3倍)和痛觉超敏(0.5倍),减轻了抑郁(0.5倍),并增强了运动协调性(1.2倍)。它减轻了组织病理学改变,并使大鼠丘脑内的多巴胺水平提高了88.5%。莫达非尼通过抑制肥大细胞和小胶质细胞活化发挥抗炎作用,表现为速激肽/ MRGPRX2 /白细胞介素-17 /组胺(分别降低52%、58%、56.7%和63.7%)和PI3K / p-Akt / t-Akt / NF-κB /肿瘤坏死因子-α /白细胞介素-6(分别降低31.7%、55.5%、41%、47.6%和76.9%)。最终,莫达非尼减轻了FMS行为、组织病理学和生化异常,并抑制了利血平处理的大鼠丘脑中肥大细胞-小胶质细胞神经炎症。本研究突出了将莫达非尼重新用于改善FMS症状的潜力。