莫达非尼通过多巴胺/ P物质/MRGPRX/组胺和PI3K/ P - akt /NF-κB信号通路调节肥大细胞和小胶质细胞活化,改善大鼠纤维肌痛综合征

IF 6.2
Mennat-Allah M Kamal, Reham M Essam, Noha F Abdelkader, Hala F Zaki
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引用次数: 0

摘要

纤维肌痛综合征(FMS)的特征是长时间的、广泛的肌肉骨骼疼痛,并伴有各种生理和心理障碍。莫达非尼是一种促进清醒的药物,通过抑制多巴胺再摄取,表现出抗炎和免疫调节作用,包括细胞因子产生、小胶质细胞和肥大细胞活化的损害,来控制几种疾病的疼痛症状。中枢性炎症可能涉及与肥大细胞激活相关的小胶质细胞激活。恢复多巴胺水平和调节肥大细胞和小胶质细胞之间的交流可能是治疗FMS疼痛症状的一种有希望的方法。因此,本研究旨在探讨脑肥大细胞与小胶质细胞之间的相互作用作为FMS病理生理的潜在机制,以及莫达非尼如何控制这种相互作用,重点关注多巴胺/SP/MRGPRX2/组胺和PI3K/p-Akt/NF-κB信号通路。将大鼠随机分为4组。第1组为正常对照。利血平(1mg /kg/天;S.c)连续3天注射到其余各组。3、4组:莫达非尼(100 mg/kg/天;P.o)单独或与氟哌啶醇联合使用(1mg /kg/天;),在接下来的21天内分别进行试验。莫达非尼改善利血平引起的热/机械异常性痛(1.3倍,2.3倍)和痛觉过敏(0.5倍),减轻抑郁(0.5倍),增强运动协调(1.2倍)。它减轻了大鼠丘脑的组织病理学改变,并使多巴胺水平增加了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SP/MRGPRX2/IL-17/组胺(52%、58%、56.7%和63.7%)和PI3K/p-Akt/t-Akt/NF-κB/TNF-α/IL-6(31.7%、55.5%、41%、47.6%和76.9%)的降低。最终,莫达非尼减轻了利血平暴露大鼠FMS行为、组织病理学和生化异常,并抑制了丘脑肥大细胞-小胶质神经炎症。这项研究强调了重新利用莫达非尼改善FMS症状的潜力。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Modafinil Ameliorated Fibromyalgia Syndrome in Rats by Modulating Mast Cells and Microglia Activation Through Dopamine/Substance P/MRGPRX/Histamine and PI3K/p-Akt/NF-κB Signaling Pathways.

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.

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