Hyperglycemia induced C2C12 myoblast cell cycle arrest and skeletal muscle atrophy by modulating sirtuins gene expression in rats

• DOI: 10.24425/pjvs.2021.139981
• Publication Date: 2023-07-20T19:01:33Z
• Authors: P. Surinlert; T. Thitiphatphuvanon; W. Khimmaktong; C. Pholpramool; C. Tipbunjong
• Keywords: C2C12; Muscle Atrophy

Diabetes is characterized by high blood glucose level termed hyperglycemia affecting skeletal muscle structure and function an unclear molecular mechanism.This study aimed to investigate the effect underlying mechanism(s) of on both in vitro vivo.Treatment with hyperglycemic condition (25 mM) for 48 h significantly inhibited C2C12 myoblast proliferation detected MTT assay whilst flow cytometry revealed interruption cell cycle at subG1 G2/M phases.An exposure decreased myosin heavy chain (MHC) protein expression differentiated myotube tibialis anterior (TA) Wistar rats.In addition, cross-section area (MCA) TA diabetic rats were compared non-diabetic control.Western blotting analysis myoblasts myotubes increased expressions cleaved-caspase-9 cleaved-caspase-3, but not cleaved-caspase-8.Of note, these caspases muscles changed under condition.Quantitative real-time polymerase reaction (qRT-PCR) modulation gene sirtuins (SIRTs).In myoblasts, SIRT1, SIRT2 SIRT4 upregulated SIRT7 was downregulated.Meanwhile, downregulated.Taken together, this showed that induced arrest apoptosis degradation atrophy most likely via SIRTs expression.