Ibuprofen does not impair skeletal muscle regeneration upon cardiotoxin-induced injury

Title:

Ibuprofen does not impair skeletal muscle regeneration upon cardiotoxin-induced injury

Creator:

Dalle, Sebastiaan, Poffé, Chiel, Hiroux, Charlotte, Suhr, Frank, Deldicque, Louise, and Koppo, Katrien

Identifier:

https://cdk.lib.cas.cz/client/handle/uuid:1b831b4e-16a3-4de4-b295-89927c64f9a7
uuid:1b831b4e-16a3-4de4-b295-89927c64f9a7
issn:0862-8408
doi:10.33549/physiolres.934482

Subject:

záněty, cyklooxygenáza 2, inflammations, cyclooxygenase 2, NSAID, mTORC1 signaling, muscle recovery, 14, and 612

Type:

model:article and TEXT

Format:

počítač and online zdroj

Description:

Muscle regeneration is regulated through interaction between muscle and immune cells. Studies showed that treatment with supra-physiological doses of Non-Steroidal Anti-Inflammatory Drug (NSAID) abolished inflammatory signaling and impaired muscle recovery. The present study examines the effects of pharmacologically-relevant NSAID treatment on muscle regeneration. C57BL/6 mice were injected in the tibialis anterior (TA) with either PBS or cardiotoxin (CTX). CTX-injected mice received ibuprofen (CTX-IBU) or were untreated (CTX-PLAC). After 2 days, Il-1β and Il-6 expression was upregulated in the TA of CTX-IBU and CTX-PL vs. PBS. However, Cox-2 expression and macrophage infiltration were higher in CTX-PL vs. PBS, but not in CTX-IBU. At the same time, anabolic markers were higher in CTX-IBU vs. PBS, but not in CTX-PL. Nevertheless, ibuprofen did not affect muscle mass or muscle fiber regeneration. In conclusion, mild ibuprofen doses did not worsen muscle regeneration. There were even signs of a transient improvement in anabolic signaling and attenuation of inflammatory signaling., Sebastiaan Dalle, Chiel Poffé, Charlotte Hiroux, Frank Suhr, Louise Deldicque, Katrien Koppo., and Obsahuje bibliografii

Language:

English

Rights:

http://creativecommons.org/publicdomain/mark/1.0/
policy:public

Coverage:

847-859

Source:

Physiological research | 2020 Volume:69 | Number:5

Harvested from:

CDK

Metadata only:

false