Apoptotic changes and myofibrils degradation in post-mortem chicken muscles by ultrasonic processing

In this study, 1500 W, 40 kHz ultrasound was used to treat chicken muscle during 5 days of ageing after slaughter. Ultrasound treatment-induced typical apoptosis was applied to chicken muscle after slaughter. Our Western blot results showed that the key factors of the death receptor pathway in apoptosis fas, fas-L, and caspase-8 were activated during storage of the meat. Treatment with ultrasound significantly stimulated the activity of caspase-9, cytochrome c and tbid, and increased the ratio of bax/bcl-2 as shown by western blotting analysis. Transmission electron microscopy images showed ultrastructural damage to the mitochondria and nucleus that was morphologically characteristic of apoptosis during post-mortem ageing. All the treatments reduced the band intensity of desmin and caspase-3 during 5 days of meat ageing. The hematoxylin-eosin staining of muscle tissue structure showed that ultrasound treatment increased the gap between muscle fibre bundles. Ultrasonic treatment significantly reduced the shear force of chicken breast, which could improve the tenderness of the meat. The findings of this investigation revealed that ultrasound affected meat ageing via apoptosis and possibly activated myofibril degradation. We speculate that the morphological and biochemical changes relating to apoptosis have the potential to contribute to the tenderization of meat. •Ultrasound improved tenderness and increased the gap between muscle fibre bundles of chicken meat.•Ultrasound activate apoptosis, which was induced by the mitochondria/death-receptor pathways.•Higher caspase-8, caspase-3 activity, and enhanced of fas, fas-L occurred.•Caspase-9 was activated, and cytochrome c, tbid and ratio of bax/bcl-2 were increased.•Mitochondrial damage and condensation of nuclear chromatin occurred.