Sun Jinghe, Yan Tingting, Wang Xiaoyan, Li Yimeng, Yang Jingfeng
School of Food Science and Technology, National Engineering Research Center of Seafood, Dalian Polytechnic University, Dalian 116034, PR China.
National & Local Joint Engineering Laboratory for Marine Bioactive Polysaccharide Development and Application, Dalian Polytechnic University, Dalian 116034, PR China.
J Agric Food Chem. 2025 Jan 22;73(3):2197-2214. doi: 10.1021/acs.jafc.4c10292. Epub 2025 Jan 9.
This study aims to reveal the transduction signaling network that triggers sea cucumber () autolysis. The tandem mass tag (TMT) proteomics and transcriptomic techniques were used to analyze expression differences between inhibited and activated sea cucumber autolysis. Flow cytometry was used to identify apoptosis. Western blotting and RT-PCR verified the signaling pathway. The results showed that the angiotensin-converting enzyme 2 (ACE 2) activator (diminazene, DIZE) maintained the health of . The ACE 2 inhibitor (captopril, Capt) accelerated the autolysis. Based on the multiomics analysis, the ACE 2 activator activated the downstream NF-κB pathway to prevent the sea cucumber apoptosis. The Capt activated apoptosis initiation. Apoptosis occurred through the regulation of TNF and PI3K-Akt signaling pathways, which downregulate NF-κB. Akt was identified as an intermediate signaling protein downstream of ACE 2 that regulates autolysis in . Compared to in the ultraviolet-irradiated and Capt groups, the Akt inhibitor (perifosine, KRX) significantly reduced the expression of the PI3K-Akt and NF-κB pathways, thereby inhibiting the autolysis process. Additionally, DIZE attenuated ROS levels, thereby inhibiting the autolysis of . This study provides better insight into the autolysis mechanism of .
本研究旨在揭示触发海参自溶的转导信号网络。采用串联质谱标签(TMT)蛋白质组学和转录组学技术分析抑制和激活海参自溶之间的表达差异。使用流式细胞术鉴定细胞凋亡。蛋白质免疫印迹法和逆转录聚合酶链反应验证了信号通路。结果表明,血管紧张素转换酶2(ACE 2)激活剂(地美硝唑,DIZE)维持了海参的健康。ACE 2抑制剂(卡托普利,Capt)加速了自溶。基于多组学分析,ACE 2激活剂激活下游NF-κB通路以防止海参细胞凋亡。Capt激活凋亡起始。凋亡通过调节肿瘤坏死因子(TNF)和磷脂酰肌醇-3激酶-蛋白激酶B(PI3K-Akt)信号通路发生,这些通路下调NF-κB。Akt被确定为ACE 2下游调节海参自溶的中间信号蛋白。与紫外线照射组和Capt组的海参相比,Akt抑制剂(哌立福辛,KRX)显著降低了PI3K-Akt和NF-κB通路的表达,从而抑制了自溶过程。此外,DIZE降低了活性氧水平,从而抑制了海参的自溶。本研究为海参的自溶机制提供了更好的见解。