摘要
The degradation of structural proteins during fish postmortem storage is a critical factor affecting meat quality,leading to economic losses in the seafood industry.The complex interplay between caspase-3 and structural protein stability during fish postmortem storage remains largely unexplored.By treating grass carp fillets with a caspase-3 inhibitor,we establish a model for inhibiting apoptosis,delineating the role of caspase-3 in protein degradation.The effect of caspase-3 on grass carp proteins following postmortem storage and its cascade interaction with calpain and cathepsin L was further investigated.The result demonstrated that the destabili-zation of the mitochondrial membrane during apoptosis led to modifications in the B-cell lymphoma(Bcl)family proteins,subsequently triggered the activation of caspase-9/caspase-3.Additionally,caspase-3 reduced the expression of the calpastatin and lysosomal membrane protein 1(LAMP-1)gene,resulting in increased calpain and cathepsin L activity.SDS-PAGE and liquid chromatography-tandem mass spectrometry(LC-MS/MS)analysis indicated that caspase-3 inhibitor treatment reduced actin fractures and preserved critical structural proteins.This investigation unveils the molecular mechanisms through which caspase-3 affects protein degradation in fish fillets during storage,providing valuable insights into the postmortem degradation processes.
基金
supported by the National Natural Science Foundation of China(award No.32372397)
the China Agriculture Research System of MOF and MARA(CARS-45)
The Figs.5(G)and Fig.7(D)were created with icons provided by Biorender(https://biorender.com)(Agreement number:MY2617L6ID,YG2617LFWE).
