伊诺斯
纤维肌痛
非西汀
医学
内科学
内分泌学
氧化应激
自噬
内皮功能障碍
病理
一氧化氮
细胞凋亡
生物
一氧化氮合酶
抗氧化剂
类黄酮
生物化学
作者
Fatma M Ghoneim,Salwa Mohamed Abo-Elkhair,Ayman Z. Elsamanoudy,Dalia A. Shabaan
出处
期刊:Cells
[MDPI AG]
日期:2021-12-24
卷期号:11 (1): 48-48
被引量:3
标识
DOI:10.3390/cells11010048
摘要
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.
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