文献类型：期刊文献

英文题名：Pacific Oyster-Derived Alcohol Dehydrogenase Activating Peptide Leu-Gln-Pro-Pro-Arg Ameliorates Alcoholic Liver Disease by Enhancing Alcohol Metabolism and Suppressing Mitochondrial-Mediated Apoptosis

作者：Chen, Yajing[1];Zhang, Xiuli[1];Gao, Jialong[1,2];Cao, Wenhong[1,2];Qin, Xiaoming[1,2];Lin, Haisheng[1,2];Chen, Zhongqin[1,2];Zheng, Huina[1,2];Zhu, Guoping[1,2];Zheng, Zhihong[1,2]

机构：[1]Guangdong Ocean Univ, Coll Food Sci & Technol,Guangdong Prov Key Lab Aqu, Guangdong Prov Engn Technol Res Ctr Seafood, Guangdong Prov Engn Technol Res Ctr Prefabricated, Zhanjiang 524088, Peoples R China;[2]Dalian Polytech Univ, Collaborat Innovat Ctr Seafood Deep Proc, Dalian 116034, Peoples R China

年份：2025

卷号：73

期号：34

起止页码：21422

外文期刊名：JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY

收录：SCI-EXPANDED(收录号：WOS:001552035400001)、、EI(收录号：20253519085396)、Scopus(收录号：2-s2.0-105014226109)、WOS

基金：This work was supported by the special funds for the Construction of Modern Agricultural Industrial Technology System (Grant numbers: CARS-49) and Research Initiation Project of Guangdong Ocean University (grant number: 060302042407). The authors thank Figdraw (www.figdraw.com) of Home for Researchers for technical support (Figure ID: UUIIY346b4, UPTRRa9ea9, and UPURSdd933).

语种：英文

外文关键词：alcoholic liver disease; alcohol metabolism; mitochondria; apoptosis; ADH-activating peptide

外文摘要：Alcohol dehydrogenase (ADH) plays an important role in improving alcohol metabolism. Bioactive peptides, as functional factors with low toxicity and easy absorption, have attracted increasing attention in the intervention of alcoholic liver disease (ALD). This study investigated the effects of LQPPR, an ADH-activating peptide from Pacific oysters, on ALD and further elucidated its mechanism. The results indicated that LQPPR can reduce serum transaminase levels, ameliorate alcohol-induced liver histopathological changes, and exert a notable protective effect against ALD. From the perspective of alcohol metabolism, LQPPR enhanced ADH and ALDH activity while reducing CYP2E1 expression levels, thereby decreasing ROS and MDA content, improving SOD and GSH levels, and mitigating oxidative damage to hepatocyte mitochondria. Furthermore, LQPPR improved mitochondrial function by reducing oxidative damage, subsequently alleviating alcohol-induced disruptions in ATP and NADH/NAD+ levels. This downregulated the expression of Bax, cytochrome c, and cleaved caspase-3 in the liver, ultimately inhibiting the mitochondrial-mediated apoptosis pathway and exerting hepatoprotective effects. In summary, the ADH-activating peptide LQPPR can reduce hepatic oxidative damage by modulating alcohol metabolism, thereby preventing mitochondrial dysfunction and suppressing the mitochondrial-mediated apoptosis pathway. These results suggest that LQPPR may serve as a potential functional component for the prevention of ALD.