Pioglitazone improves skeletal muscle functions in reserpine-induced fibromyalgia rat model

Fibromyalgia (FM) is characterized by musculoskeletal pain, fatigue, sleep and memory disturbance. There is no definitive cure yet for FM-related health problems. Peroxisome proliferator-activated receptor's (PPAR's) activation is associated with insulin sensitisation and improved glucose...

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Published inAnnals of medicine (Helsinki) Vol. 53; no. 1; pp. 1033 - 1041
Main Authors Hassan, Fatma E., Sakr, Hader I., Mohie, Passant M., Suliman, Howayda Saeed, Mohamed, Ayman Saber, Attia, Mohamed H., Eid, Dalia M.
Format Journal Article
LanguageEnglish
Published England Taylor & Francis 01.01.2021
Taylor & Francis Group
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Summary:Fibromyalgia (FM) is characterized by musculoskeletal pain, fatigue, sleep and memory disturbance. There is no definitive cure yet for FM-related health problems. Peroxisome proliferator-activated receptor's (PPAR's) activation is associated with insulin sensitisation and improved glucose metabolism. PPAR-γ was reported to alleviate FM allodynia. Limited data are discussing its effect on motor disorders. To investigate the potential effect of PPAR-γ agonists (pioglitazone, as one member of thiazolidinediones (TZD)) on motor dysfunction in reserpine-induced FM in a rat model. Thirty-six male Wistar rats were divided into negative control (n = 9) and reserpine-induced FM (n = 27) groups. The latter was subdivided into three equal subgroups (n = 9), positive control (untreated FM model), pioglitazone-treated and GW9662-treated. We evaluated muscle functions and activity of chloramphenicol acetyltransferase, superoxide dismutase, malondialdehyde, and serum levels of interleukin-8 and monocyte chemoattractant protein-1. Pioglitazone significantly relieved fatigue, improved muscle performance, reduced inflammatory cytokines and enhanced antioxidant's activity, while GW9662, a known PPAR-γ antagonist, aggravated the FM manifestations in the rat model. PPAR-γ agonists show a promising role against FM-associated motor dysfunctions.
ISSN:0785-3890
1365-2060
DOI:10.1080/07853890.2021.1916069