Entacapone alleviates muscle atrophy by modulating oxidative stress, proteolysis, and lipid aggregation in multiple mice models DOI Creative Commons

Rong Zeng,

Hanbing Xu,

Mingzheng Wu

и другие.

Frontiers in Physiology, Год журнала: 2024, Номер 15

Опубликована: Дек. 9, 2024

Background Skeletal muscle atrophy significantly affects quality of life and has socio-economic health implications. This study evaluates the effects entacapone (ENT) on skeletal linked with oxidative stress proteolysis. Methods C2C12 cells were treated dexamethasone (Dex) to simulate atrophy. Four murine models employed: diaphragm from mechanical ventilation, Dex-induced atrophy, lipopolysaccharide (LPS)-induced hyperlipidemia-induced Each model utilized (10 mg/kg), sample sizes: Control (9), MV (11), + ENT (5) for atrophy; (4), Dex model; LPS similar hyperlipidemia. Measurements included strength, myofiber cross-sectional area (CSA), proteolysis, markers [uperoxide dismutase 1 (SOD1), uperoxide 2 (SOD2), 4-hydroxynonenal (4-HNE)], lipid levels. Results Our findings confirm evidenced by increased expression atrophy-associated proteins, including Atrogin-1 Murf-1, along decreased diameter myotubes. levels rose 660.6% ( p < 0.05) in group compared control, while reduced 84.4% 0.05). Similarly, Murf-1 365% 89.5% entacapone. Dexamethasone exposure induces stress, upregulation stress-related proteins Sod1, Sod2, 4-HNE. Entacapone these markers, enhancing GSH-PX content 385.6% Dex-treated group. Additionally, effectively increase MDA 63.98% Furthermore, prevents decline strength CSA mice. It also mitigates protein hydrolysis. exhibits ability attenuate accumulation gastrocnemius hyperlipidemic mice alleviate reduction fiber CSA. Conclusion suggest that is a promising therapeutic candidate functioning through aggregation. Future research should explore underlying mechanisms potential clinical applications muscle-wasting conditions.

Язык: Английский

Entacapone alleviates muscle atrophy by modulating oxidative stress, proteolysis, and lipid aggregation in multiple mice models DOI Creative Commons

Rong Zeng,

Hanbing Xu,

Mingzheng Wu

и другие.

Frontiers in Physiology, Год журнала: 2024, Номер 15

Опубликована: Дек. 9, 2024

Background Skeletal muscle atrophy significantly affects quality of life and has socio-economic health implications. This study evaluates the effects entacapone (ENT) on skeletal linked with oxidative stress proteolysis. Methods C2C12 cells were treated dexamethasone (Dex) to simulate atrophy. Four murine models employed: diaphragm from mechanical ventilation, Dex-induced atrophy, lipopolysaccharide (LPS)-induced hyperlipidemia-induced Each model utilized (10 mg/kg), sample sizes: Control (9), MV (11), + ENT (5) for atrophy; (4), Dex model; LPS similar hyperlipidemia. Measurements included strength, myofiber cross-sectional area (CSA), proteolysis, markers [uperoxide dismutase 1 (SOD1), uperoxide 2 (SOD2), 4-hydroxynonenal (4-HNE)], lipid levels. Results Our findings confirm evidenced by increased expression atrophy-associated proteins, including Atrogin-1 Murf-1, along decreased diameter myotubes. levels rose 660.6% ( p < 0.05) in group compared control, while reduced 84.4% 0.05). Similarly, Murf-1 365% 89.5% entacapone. Dexamethasone exposure induces stress, upregulation stress-related proteins Sod1, Sod2, 4-HNE. Entacapone these markers, enhancing GSH-PX content 385.6% Dex-treated group. Additionally, effectively increase MDA 63.98% Furthermore, prevents decline strength CSA mice. It also mitigates protein hydrolysis. exhibits ability attenuate accumulation gastrocnemius hyperlipidemic mice alleviate reduction fiber CSA. Conclusion suggest that is a promising therapeutic candidate functioning through aggregation. Future research should explore underlying mechanisms potential clinical applications muscle-wasting conditions.

Язык: Английский

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