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Protective effects of Salubrinal against H2O2-induced muscle wasting via eIF2α/ATF4 signaling pathway
Siming Lin1,2,3, Jingying Wu3, Guili Lian3
1Department of Emergency, The First Affiliated Hospital, Fujian Medical University, Fuzhou, China.
Background:
Endoplasmic reticulum stress (ERS) plays a critical role in skeletal muscle physiology and pathology, though the precise mechanisms remain unclear. Salubrinal, a selective inhibitor of eIF2α dephosphorylation, has been shown as a potential therapeutic agent for various conditions, but its effects on sarcopenia are not well understood. This study investigated the protective effects of salubrinal against H2O2-induced muscle cell injury and its impact on the eIF2α/ATF4 signaling pathway.
Methods:
Gastrocnemius muscle samples from aged mice were used and cultured C2C12 myotubes were also used to explore the effects of Salubrinal through Western blotting, immunofluorescence, and apoptosis assays.
Results:
Our results demonstrated that H2O2 treatment induced significant muscle cell damage, evidenced by reduced MHC1 expression and increased apoptosis. Salubrinal, in a concentration-dependent manner, mitigated these effects, preserving MHC1 expression and reducing apoptosis. Furthermore, salubrinal enhanced the expression of p-eIF2α and ATF4, suggesting that its protective effects are mediated through the eIF2α/ATF4 pathway.
Conclusion:
These findings highlight salubrinal's potential as a therapeutic agent for muscle wasting conditions, particularly those related to oxidative stress and ERS.
