Centro Andaluz de Biología del Desarrollo (CABD), Universidad Pablo de Olavide-CSIC, Ctra, de Utrera, km, 1, ISCIII, Sevilla 41013, Spain.
Arthritis Res Ther. 2010;12(1):R17. doi: 10.1186/ar2918. Epub 2010 Jan 28.
Fibromyalgia is a chronic pain syndrome with unknown etiology. Recent studies have shown some evidence demonstrating that oxidative stress may have a role in the pathophysiology of fibromyalgia. However, it is still not clear whether oxidative stress is the cause or the effect of the abnormalities documented in fibromyalgia. Furthermore, the role of mitochondria in the redox imbalance reported in fibromyalgia also is controversial. We undertook this study to investigate the role of mitochondrial dysfunction, oxidative stress, and mitophagy in fibromyalgia.
We studied 20 patients (2 male, 18 female patients) from the database of the Sevillian Fibromyalgia Association and 10 healthy controls. We evaluated mitochondrial function in blood mononuclear cells from fibromyalgia patients measuring, coenzyme Q10 levels with high-performance liquid chromatography (HPLC), and mitochondrial membrane potential with flow cytometry. Oxidative stress was determined by measuring mitochondrial superoxide production with MitoSOX and lipid peroxidation in blood mononuclear cells and plasma from fibromyalgia patients. Autophagy activation was evaluated by quantifying the fluorescence intensity of LysoTracker Red staining of blood mononuclear cells. Mitophagy was confirmed by measuring citrate synthase activity and electron microscopy examination of blood mononuclear cells.
We found reduced levels of coenzyme Q10, decreased mitochondrial membrane potential, increased levels of mitochondrial superoxide in blood mononuclear cells, and increased levels of lipid peroxidation in both blood mononuclear cells and plasma from fibromyalgia patients. Mitochondrial dysfunction was also associated with increased expression of autophagic genes and the elimination of dysfunctional mitochondria with mitophagy.
These findings may support the role of oxidative stress and mitophagy in the pathophysiology of fibromyalgia.
纤维肌痛是一种病因不明的慢性疼痛综合征。最近的研究表明，一些证据表明氧化应激可能在纤维肌痛的病理生理学中起作用。然而，目前尚不清楚氧化应激是纤维肌痛中异常的原因还是结果。此外，线粒体在纤维肌痛中报道的氧化还原失衡中的作用也存在争议。我们进行这项研究是为了探讨线粒体功能障碍、氧化应激和自噬在纤维肌痛中的作用。
我们从塞维利亚纤维肌痛协会的数据库中研究了 20 名患者（2 名男性，18 名女性患者）和 10 名健康对照者。我们通过高效液相色谱法（HPLC）测量辅酶 Q10 水平，通过流式细胞术测量线粒体膜电位，评估纤维肌痛患者血液单核细胞中的线粒体功能。通过测量纤维肌痛患者血液单核细胞和血浆中的线粒体超氧化物产生和脂质过氧化来确定氧化应激。通过量化血液单核细胞中 LysoTracker Red 染色的荧光强度来评估自噬激活。通过测量柠檬酸合酶活性和血液单核细胞的电子显微镜检查来证实自噬。
我们发现纤维肌痛患者血液单核细胞中的辅酶 Q10 水平降低，线粒体膜电位降低，线粒体超氧化物水平升高，血液单核细胞和血浆中的脂质过氧化水平升高。线粒体功能障碍还与自噬基因的表达增加以及通过自噬消除功能失调的线粒体有关。
这些发现可能支持氧化应激和自噬在纤维肌痛病理生理学中的作用。
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