死后草鱼肌肉细胞凋亡机制及相关信号通路研究

Abstract

BACKGROUND Apoptosis activation is an essential research to reveal the triggering mechanism of flesh quality deterioration. This study was aimed at explaining apoptotic mechanism of postmortem fish in terms of caspases activation, cytochrome c (cyt-c) release, B-cell lymphoma 2 (Bcl-2) and Bcl2-associated X (Bax) protein levels, transcriptional levels of its molecules, and apoptosis-inducing factor (AIF) translocation at 4 °C for 5 days. RESULTS Activation of caspase-9, caspase-8, caspase-3 and the release of mitochondrial cyt-c were observed during storage. The decreased Bcl-2 protein levels, increased Bax protein expressions and Bax/Bcl-2 ratio were major steps for inducing apoptosis. Collectively, transcriptional regulation of Fas ligand (FasL), apoptotic protease activating factor-1 (Apaf-1), inhibitors of apoptosis proteins (IAPs), myeloid cell leukemia-1 (Mcl-1), c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPK) indicated that extrinsic apoptotic pathways (FasL/caspase-8/caspase-3) and intrinsic pathway [(JNK and p38 MAPK)/(Bcl-2, Bax and Mcl-1)/cyt-c/Apaf-1/caspase-9/caspase-3] were involved in apoptotic process. Mitochondrial AIF translocation to nuclear indicated that AIF mediated caspase-independent pathway. CONCLUSION Therefore, transcriptional and translational alterations of multiple signaling molecules acted important roles in regulating apoptosis activation in postmortem process. © 2022 Society of Chemical Industry.