AboTaleb Hanin Abdulbaset, Alturkistani Hani A, Abd El-Aziz Gamal S, Hindi Emad A, Halawani Mervat M, Al-Thepyani Mona Ali, Alghamdi Badrah S
Department of Physiology, Faculty of Medicine, King Abdulaziz University, Jeddah 21589, Saudi Arabia.
Neuroscience and Geroscience Research Unit, King Fahd Medical Research Center, King Abdulaziz University, Jeddah 21589, Saudi Arabia.
Cells. 2024 Nov 30;13(23):1986. doi: 10.3390/cells13231986.
Fibromyalgia (FM) is a chronic and debilitating condition characterized by diffuse pain, often associated with symptoms such as fatigue, cognitive disturbances, and mood disorders. Metformin, an oral hypoglycemic agent, has recently gained attention for its potential benefits beyond glucose regulation. It has shown promise in alleviating neuropathic and inflammatory pain, suggesting that it could offer a novel approach to managing chronic pain conditions like FM. This study aimed to further explore metformin's analgesic potential by evaluating its effects in an experimental FM model induced by reserpine in both male and female mice. After the administration of 200 mg/kg metformin to male and female mice, the FM-related symptoms were assessed, including mechanical allodynia, thermal hyperalgesia, and depressive-like behaviors. A histological examination of the thalamus, hippocampus, and spinal cord was conducted using haematoxylin and eosin staining. The neurotransmitter and proinflammatory cytokines levels were measured in the brains and spinal cords. Our results have shown that metformin treatment for seven days significantly reversed these FM-like symptoms, reducing pain sensitivity and improving mood-related behaviors in both the male and female mice. Additionally, metformin exhibited neuroprotective effects, mitigating reserpine-induced damage in the hippocampus, thalamus, and spinal cord. It also significantly lowered the levels of the proinflammatory cytokine interleukin 1-beta (IL-1β) in the brain and spinal cord. Notably, metformin modulated the neurotransmitter levels differently between the sexes, decreasing glutamate and increasing serotonin and norepinephrine in the male mice, but not in the females. These findings underscore metformin's potential as an alternative therapy for FM, with sex-specific differences suggesting distinct mechanisms of action.
纤维肌痛(FM)是一种慢性致残性疾病,其特征为弥漫性疼痛,常伴有疲劳、认知障碍和情绪障碍等症状。二甲双胍是一种口服降糖药,最近因其在血糖调节之外的潜在益处而受到关注。它在减轻神经性和炎症性疼痛方面显示出前景,这表明它可能为管理像纤维肌痛这样的慢性疼痛疾病提供一种新方法。本研究旨在通过评估二甲双胍在利血平诱导的雄性和雌性小鼠实验性纤维肌痛模型中的作用,进一步探索其镇痛潜力。给雄性和雌性小鼠施用200mg/kg二甲双胍后,评估与纤维肌痛相关的症状,包括机械性异常性疼痛、热痛觉过敏和抑郁样行为。使用苏木精和伊红染色对丘脑、海马和脊髓进行组织学检查。测量大脑和脊髓中的神经递质和促炎细胞因子水平。我们的结果表明,二甲双胍治疗七天可显著逆转这些类似纤维肌痛的症状,降低雄性和雌性小鼠的疼痛敏感性并改善与情绪相关的行为。此外,二甲双胍表现出神经保护作用,减轻利血平诱导的海马、丘脑和脊髓损伤。它还显著降低大脑和脊髓中促炎细胞因子白细胞介素1-β(IL-1β)的水平。值得注意的是,二甲双胍对不同性别的神经递质水平调节不同,在雄性小鼠中降低谷氨酸水平并增加血清素和去甲肾上腺素水平,但在雌性小鼠中则不然。这些发现强调了二甲双胍作为纤维肌痛替代疗法的潜力,性别特异性差异表明其作用机制不同。