FOOD SCIENCE ›› 2024, Vol. 45 ›› Issue (6): 48-54.doi: 10.7506/spkx1002-6630-20230519-194

• Bioengineering • Previous Articles     Next Articles

Effect of Basigin on the Mitogen Activated Protein Kinase Signaling Pathway and Apoptosis in Qinchuan Cattle Muscle during Postmortem Maturation

SU Xiaofeng, LI Yalei, LUO Ruiming   

  1. (School of Food Science and Engineering, Ningxia University, Yinchuan 750021, China)
  • Online:2024-03-25 Published:2024-04-03

Abstract: In order to explore the effects of basigin (BSG) on the mitogen activated protein kinase (MAPK) signaling pathway and apoptosis in Qinchuan cattle muscle during postmortem maturation, the changes in BSG and related differentially expressed proteins were analyzed by 4D-label free quantification (4D-LFQ). The BSG inhibitor tunicamycin was injected into the longissimus dorsi of Qinchuan cattle after slaughter, and the expression levels of key proteins in the MAPK signaling pathway during storage at 4 ℃ were determined by Western blotting. An apoptosis detection kit was used to determine the change in the activity of caspase-3. The results showed that the expression of BSG increased first and then decreased during the postmortem storage period of Qinchuan cattle muscle. Through Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis, it was found that BSG and related differentially expressed proteins were significantly annotated to the oxidative phosphorylation pathway, calcium signal pathway and MAPK signaling pathway, indicating that BSG played an important role through the MAPK signaling pathway. In addition, for the tunicamycin group, the relative expression of the key proteins in the MAPK signaling pathway was significantly down-regulated, indicating that BSG inactivated the MAPK signaling pathway. This finding lays a good foundation for exploring the effect of BSG on the MAPK signaling pathway. After inhibiting BSG expression, caspase-3 activity in the tunicamycin group increased significantly, indicating that apoptosis was an important link in cell injury mechanism, and tunicamycin acted on the N-terminal structure of BSG to deglycosylate the protein and inhibited the folding of intracellular proteins and consequently their biological activity, thereby inducing cell apoptosis.

Key words: Qinchuan cattle longissimus dorsi; mitogen activated protein kinase signaling pathway; tunicamycin; apoptosis; cell damage

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