Abstract
Fibromyalgia (FM) is a common chronic pain syndrome that affects 1% to 5% of the population. We aimed to investigate the role of endothelial dysfunction and autophagy in fibromyalgia-related vascular and cerebral cortical changes in a reserpine-induced rat model of fibromyalgia at the histological and molecular levels and to study the ameliorative effect of fisetin. Forty adult female albino rats were divided into four groups (10 each): two control groups, the reserpine-induced fibromyalgia group, and the fisetin-treated group. The carotid arteries and brains of the animals were dissected. Frozen tissue samples were used for total RNA extraction and qPCR analysis of eNOS, caspase-3, Bcl-2, LC-3, BECN-1, CHOP, and TNF-α expression. Histological, immunohistochemical (eNOS), and ultrastructure studies were conducted. The carotid arteries revealed excessive autophagy and endothelial, vascular, and apoptotic changes. The cerebral cortex showed similar findings apart from endoplasmic reticulum stress. Additionally, there was decreased gene expression of eNOS and Bcl-2 and increased expression of caspase-3, LC-3, BECN-1, CHOP, and TNF-α. In the fisetin-treated rats, improvements in the histological and molecular results were detected. In conclusion, oxidative stress, enhanced apoptosis, and excessive autophagy are fundamental pathophysiologic mechanisms of reserpine-induced fibromyalgia. Moreover, fisetin has an ameliorative effect against fibromyalgia.
Highlights
Published: 24 December 2021Fibromyalgia (FM) is a common and complex chronic pain syndrome that affects 1%to 5% of the population [1]
There were degenerative changes in the form of foam cells in the tunica media, some smooth muscle cells appeared with plump nuclei, and others appeared with dark pyknotic nuclei (Figure 1B)
The reserpine-induced fibromyalgia group showed a significant increase in serum MDA and nitric oxide (NO) levels, with a significant decrease in the total antioxidant capacity (TAC)
Summary
Published: 24 December 2021Fibromyalgia (FM) is a common and complex chronic pain syndrome that affects 1%to 5% of the population [1]. Fibromyalgia (FM) is a common and complex chronic pain syndrome that affects 1%. The most common characteristic of fibromyalgia is chronic and prevalent pain without any apparent organic lesion that lasts for more than three months. There are inconsistencies in the pathogenesis of FM, and the source of sensory inputs is unknown [4]; some hypotheses on peripheral and central pathophysiological mechanisms have been suggested. Endothelial dysfunction (ED) is a well-established risk factor that plays a pathophysiologic role in the development of atherosclerosis and in related disorders. ED has been shown to develop in different conditions, such as diabetes mellitus, arterial hypertension, chronic heart failure, and stroke [5]. It has previously been proposed that ED participates in the pathophysiology of fibromyalgia and fibromyalgia-related disorders [6]
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