Anatomy and Physiopathology Division, Department of Clinical and Experimental Sciences, University of Brescia, Viale Europa 11, 25123 Brescia, Italy.
Interdipartimental University Center of Research "Adaption and Regeneration of Tissues and Organs-(ARTO)", University of Brescia, 25123 Brescia, Italy.
Int J Mol Sci. 2019 Feb 11;20(3):765. doi: 10.3390/ijms20030765.
Fibromyalgia syndrome (FMS) is considered a musculoskeletal disorder associated to other symptoms including chronic pain. Since the hypothesis of FMS etiogenesis is consistent with mitochondrial dysfunction and oxidative stress, we evaluated the pathophysiological correlation among these factors studying some proteins involved in the mitochondrial homeostasis. We focused our attention on the roles of peroxisome proliferator activated receptor gamma coactivator-1alpha (PGC-1α), mitofusin2 (Mfn2), and coenzyme Q10 (CoQ10) in reserpine-induced myalgic (RIM) rats that manifest fibromyalgia-like chronic pain symptoms. First, we underlined that RIM rats are a good model for studying the pathophysiology of FMS and moreover, we found that PGC-1α, Mfn2, and CoQ10 are involved in FMS. In fact, their expressions were reduced in gastrocnemius muscle determining an incorrect mitochondrial homeostasis. Today, none of the currently available drugs are fully effective against the symptoms of this disease and they, often, induce several adverse events; hence, many scientists have taken on the challenge of searching for non-pharmacological treatments. Another goal of this study was therefore the evaluation of the potential benefits of melatonin, an endogenous indoleamine having several functions including its potent capacity to induce antioxidant enzymes and to determine the protective or reparative mechanisms in the cells. We observed that melatonin supplementation significantly preserved all the studied parameters, counteracting oxidative stress in RIM rats and confirming that this indoleamine should be taken in consideration for improving health and/or counteract mitochondrial related diseases.
纤维肌痛综合征（FMS）被认为是一种与其他症状相关的肌肉骨骼疾病，包括慢性疼痛。由于 FMS 发病机制的假设与线粒体功能障碍和氧化应激一致，我们评估了这些因素之间的病理生理相关性，研究了一些涉及线粒体动态平衡的蛋白质。我们将注意力集中在过氧化物酶体增殖物激活受体γ共激活因子-1α（PGC-1α）、线粒体融合蛋白 2（Mfn2）和辅酶 Q10（CoQ10）在reserpine 诱导的肌痛（RIM）大鼠中的作用上，这些大鼠表现出类似纤维肌痛的慢性疼痛症状。首先，我们强调 RIM 大鼠是研究 FMS 病理生理学的良好模型，此外，我们发现 PGC-1α、Mfn2 和 CoQ10 参与了 FMS。事实上，它们在比目鱼肌中的表达减少导致了不正确的线粒体动态平衡。目前，没有一种现有的药物对这种疾病的症状完全有效，而且它们常常会引起多种不良反应；因此，许多科学家都承担起了寻找非药物治疗方法的挑战。本研究的另一个目标是评估褪黑素作为一种内源性吲哚胺的潜在益处，它具有多种功能，包括其诱导抗氧化酶的强大能力，以及在细胞中确定保护或修复机制。我们观察到褪黑素补充剂显著保存了所有研究参数，在 RIM 大鼠中对抗氧化应激，并证实这种吲哚胺应该被考虑用于改善健康和/或对抗与线粒体相关的疾病。
