In order to investigate the effects of lipopolysaccharide (LPS) on the mitochondrial signaling pathway in muscle cells of Tan sheep, M longissimus dorsi muscles from six-month-old Tan sheep were aged at 4 ℃ for 0, 6, 12, 24 and 72 h postmortem and evaluated for pH, ATP content, cell apoptosis rate, cell apoptosis-related enzyme activity, succinatedehydrogenase (SDH) activity, citrate synthase (CS) activity, B-cell lymphoma 2 (Bcl-2) family protein contents, and cytochrome c (Cyt-c) and cysteinyl aspartate specific proteinase 3 (Caspase-3) expression levels. The results showed that the apoptosis rate and Bcl-2-associated X protein (Bax)/Bcl-2 ratio in the control and LPS-induced groups were significantly increased during postmortem aging (P < 0.05). The activities of Caspase-3 and Caspase-9 increased first and then decreased. After LPS treatment, the activities of Caspase-3 and Caspase-9 were higher than those in the control group at all time points. The pH, Cyt-c reduction level and mitochondrial ATP content were significantly decreased overall (P < 0.05). The relative expression level of Cyt-c was significantly increased in both groups at 12 h postmortem, and decreased during 24–72 h in the LPS group. The content of Caspase-3 activated fragment protein in the LPS treatment group was higher than that in control group at the same time points. In conclusion, LPS could activate Caspase-3 and Caspase-9, and reduce the mitochondrial content of ATP and consequently energy metabolism level, thus affecting the activities of SDH and CS, promoting the release of Cyt-C, and increasing Bax/Bcl-2 ratio, and finally inducing cell apoptosis through the mitochondrial signaling pathway.

This research investigated the relationship between mitochondrial damage and meat tenderness of Tan sheep during postmortem aging. The M. Longissimus dorsi muscles from six-month-old Tan sheep were divided into lipopolysaccharide (LPS) treatment and blank control groups. Mitochondrial reactive oxygen species (ROS) content, membrane potential, mitochondrial permeability transition pore (MPTP) openness, mitochondrial swelling, pH, cooking loss, texture, moisture distribution, shear force and myofibril fragmentation index (MFI) in each group were measured at 0, 6, 12, 24, and 72 hours postmortem. The results showed that during postmortem aging, MPTP openness gradually increased in both groups. ROS content, cooking loss rate and MFI value showed an increasing trend as well. Mitochondrial membrane potential, pH, elasticity, T₂₂ peak area and shear force showed a decreasing trend. Hardness, chewability and cohesiveness increased at first and then decreased. Therefore, disruption of oxidative homeostasis in muscle cells of Tan sheep resulted in an increase of ROS content, which caused mitochondrial damage by inducing the opening of MPTP and decreasing mitochondrial membrane potential. Moreover, the structural changes of myofibrils shortened the gap between muscle protein molecules, resulting in increased water loss rate and poorer water retention in muscles, promoting the process of myofibril fragmentation and improving the tenderness of Tan sheep meat. Correlation analysis showed that mitochondrial damage and tenderization occurred simultaneously during the postmortem aging of Tan sheep meat, and the more serious the mitochondrial damage was, the better the tenderness was.