Abstract
Fibromyalgia is a chronic syndrome characterized by widespread musculoskeletal pain and an extensive array of other symptoms including disordered sleep, fatigue, depression and anxiety. Important factors involved in the pathogenic process of fibromyalgia are inflammation and oxidative stress, suggesting that ant-inflammatory and/or antioxidant supplementation might be effective in the management and modulation of this syndrome. Recent evidence suggests that melatonin may be suitable for this purpose due to its well known ant-inflammatory, antioxidant and analgesic effects. Thus, in the current study, the effects of the oral supplementation of melatonin against fibromyalgia-related skeletal muscle alterations were evaluated. In detail, 90 Sprague Dawley rats were randomly treated with reserpine, to reproduce the pathogenic process of fibromyalgia and thereafter they received melatonin. The animals treated with reserpine showed moderate alterations at hind limb skeletal muscles level and had difficulty in moving, together with significant morphological and ultrastructural alterations and expression of inflammatory and oxidative stress markers in the gastrocnemius muscle. Interestingly, melatonin, dose and/or time dependently, reduced the difficulties in spontaneous motor activity and the musculoskeletal morphostructural, inflammatory, and oxidative stress alterations. This study suggests that melatonin in vivo may be an effective tool in the management of fibromyalgia-related musculoskeletal morphofunctional damage.
Highlights
Fibromyalgia (FM) is a multifactorial chronic syndrome [1,2] that occurs in up to 6% of the population [3,4]; it is one of the most common pathological conditions seen in primary health care [2,5]
We initially investigated motor activity, morphological, ultrastructural and oxidative stress and inflammatory changes at skeletal muscle level to document the basis of fibromyalgia etiopathogenesis and we studied in detail the involvement of nucleotide oligomerization domain like receptor 3 (NLRP3) inflammosome in the model of this disease
The animals treated only with 0.5% glacial acetic acid or 1% ethanol dissolved in drinking water for up to 60 days showed no significant differences in food intake and body weight gain compared to untreated controls
Summary
Fibromyalgia (FM) is a multifactorial chronic syndrome [1,2] that occurs in up to 6% of the population [3,4]; it is one of the most common pathological conditions seen in primary health care [2,5]. Sprott and colleagues [14] demonstrated that patients with FM are characterized by abnormalities in muscle tissue that include increased DNA fragmentation, impaired expression of constitutive enzymes and changes in the number and size of mitochondria. Regarding this hypothesis, cyclooxygenase-1 (COX-1) seems to be a key enzyme. The decrease in mitochondrial mass and the rise in production of mitochondria derived radical oxygen species (ROS) have recently been proposed as relevant events in the fibromyalgia-related alterations [16]. In fibromyalgia patients, after ROS-mediated activation, NLRP3 promotes the production of pro-inflammatory cytokines [19]
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