While reactive oxygen species (ROS) play a role in muscle repair, excessive amounts of ROS for extended periods may lead to oxidative stress. Antioxidants, as resveratrol (RS), may reduce oxidative stress, restore mitochondrial function and promote myogenesis and hypertrophy. However, RS dose-effectiveness for muscle plasticity is unclear. Therefore, we investigated RS dose-response on C2C12 myoblast and myotube plasticity 1. in the presence and 2. absence of different degrees of oxidative stress. Low RS concentration (10 μM) stimulated myoblast cell cycle arrest, migration and sprouting, which were inhibited by higher doses (40-60 μM). RS did not increase oxidative capacity. In contrast, RS induced mitochondria loss, reduced cell viability and ROS production, and activated stress response pathways [Hsp70 and pSer36-p66(ShcA) proteins]. However, the deleterious effects of H2O2 (1000 µM) on cell migration were alleviated after preconditioning with 10 µM-RS. This dose also enhanced cell motility mediated by 100 µM-H2O2, while higher RS-doses augmented the H2O2-induced impaired myoblast regeneration and mitochondrial dehydrogenase activity. In conclusion, low resveratrol doses promoted in vitro muscle regeneration and attenuated the impact of ROS, while high doses augmented the reduced plasticity and metabolism induced by oxidative stress. Thus, the effects of resveratrol depend on its dose and degree of oxidative stress.

The impact of resveratrol and hydrogen peroxide on muscle cell plasticity shows a dose-dependent interaction.

BOSUTTI, ALESSANDRA;
2015

Abstract

While reactive oxygen species (ROS) play a role in muscle repair, excessive amounts of ROS for extended periods may lead to oxidative stress. Antioxidants, as resveratrol (RS), may reduce oxidative stress, restore mitochondrial function and promote myogenesis and hypertrophy. However, RS dose-effectiveness for muscle plasticity is unclear. Therefore, we investigated RS dose-response on C2C12 myoblast and myotube plasticity 1. in the presence and 2. absence of different degrees of oxidative stress. Low RS concentration (10 μM) stimulated myoblast cell cycle arrest, migration and sprouting, which were inhibited by higher doses (40-60 μM). RS did not increase oxidative capacity. In contrast, RS induced mitochondria loss, reduced cell viability and ROS production, and activated stress response pathways [Hsp70 and pSer36-p66(ShcA) proteins]. However, the deleterious effects of H2O2 (1000 µM) on cell migration were alleviated after preconditioning with 10 µM-RS. This dose also enhanced cell motility mediated by 100 µM-H2O2, while higher RS-doses augmented the H2O2-induced impaired myoblast regeneration and mitochondrial dehydrogenase activity. In conclusion, low resveratrol doses promoted in vitro muscle regeneration and attenuated the impact of ROS, while high doses augmented the reduced plasticity and metabolism induced by oxidative stress. Thus, the effects of resveratrol depend on its dose and degree of oxidative stress.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4308712/pdf/srep08093.pdf
File in questo prodotto:
File Dimensione Formato  
The impact of resveratrol and hydrogen peroxide on muscle cell plasticity shows a dose-dependent interaction.pdf

accesso aperto

Descrizione: pdf articolo
Tipologia: Documento in Versione Editoriale
Licenza: Digital Rights Management non definito
Dimensione 6.76 MB
Formato Adobe PDF
6.76 MB Adobe PDF Visualizza/Apri
The impact of resveratrol and hydrogen...-Supplementary information.pdf

accesso aperto

Descrizione: pdf materiale aggiuntivo
Tipologia: Documento in Versione Editoriale
Licenza: Digital Rights Management non definito
Dimensione 2.64 MB
Formato Adobe PDF
2.64 MB Adobe PDF Visualizza/Apri
The impact of resveratrol and hydrogen...-Corrigendum.pdf

accesso aperto

Descrizione: pdf errata corrige
Tipologia: Documento in Versione Editoriale
Licenza: Digital Rights Management non definito
Dimensione 890.51 kB
Formato Adobe PDF
890.51 kB Adobe PDF Visualizza/Apri

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/11368/2863917
Citazioni
  • ???jsp.display-item.citation.pmc??? 17
  • Scopus 48
  • ???jsp.display-item.citation.isi??? 47
social impact