Study on Smac promoting mitochondrial pathway apoptosis and muscle tenderization during postmortem aging of Tibetan...

Postmortem aging is one of the valid methods for meat tenderization. After animal slaughter, muscle cells primarily undergo death in the form of apoptosis. Mitochondria are affected by postmortem stress conditions and initiate the mitochondrial pathway of apoptosis, which may contribute to meat tenderization. Smac is an apoptotic factor in the mitochondria, which can promote the degradation of inhibitor of apoptosis proteins (IAPs), thus activating caspases to induce apoptosis of tumor cells via the mitochondrial pathway. However, how Smac affects mitochondrial pathway apoptosis and muscle tenderization during postmortem aging of meat has not been reported. Thus, this study sought to elucidate the role of Smac in mitochondrial pathway apoptosis and muscle tenderization during postmortem aging of Tibetan sheep meat. Tibetan sheep meat was treated with 0.1 mmol/L GDC-0152 and aged at 4 °C. The related indicators were determined subsequently. Results demonstrated that the IAPs ubiquitin ligase activity, MPTP opening degree, caspase-9/3 activity, Apoptosis protease activating factor-1 (Apaf-1) concentration, apoptosis rate and MFI value of the GDC-0152 group were markedly elevated compared to the control group, while the mitochondrial membrane potential (MMP), cytoplasmic Cyt-c reduction level, IAPs concentration and shear force value were substantially decreased (P < 0.05). Furthermore, more nuclear chromatin condensation and cell shrinkage were observed in the GDC-0152 treatment group. In conclusion, Smac could promote the degradation of IAPs, accelerate mitochondrial damage, induce Cyt-c oxidation and Apaf-1 recruitment during postmortem aging of Tibetan sheep meat, thus activating caspase-9/3, facilitating mitochondrial pathway apoptosis and effectively improving Tibetan sheep meat tenderness.