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 in | Annals of medicine (Helsinki) Vol. 53; no. 1; pp. 1033 - 1041 |
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Main Authors | , , , , , , |
Format | Journal Article |
Language | English |
Published |
England
Taylor & Francis
01.01.2021
Taylor & Francis Group |
Subjects | |
Online Access | Get full text |
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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. |
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ISSN: | 0785-3890 1365-2060 |
DOI: | 10.1080/07853890.2021.1916069 |