{"title":"虹鳟鱼副产品蛋白水解物减轻酒精诱导的肝脏氧化应激和失调的自噬","authors":"Fahimeh Hasani Zangbar , Ebrahim Najdegerami , Mojtaba Hadian , Ali Shalizar-Jalali","doi":"10.1016/j.bbrep.2025.102238","DOIUrl":null,"url":null,"abstract":"<div><h3>Background</h3><div>Chronic alcohol consumption causes irreversible liver damage. With 23 % waste from 29 million tons of annual production, rainbow trout is a valuable source of natural antioxidants. This study explores the hepatoprotective effects of rainbow trout protein hydrolysates in an alcohol-induced fatty liver disease (AFLD) rat model, focusing on autophagy, apoptosis, and oxidative stress pathways.</div></div><div><h3>Methods</h3><div>Twenty-four male rats were divided into four groups: Control (C), alcohol (A), protein hydrolysates (P), and alcohol + protein hydrolysates (AP). At the end of the experiment, liver tissue samples were collected for analysis. Oxidative stress markers, including malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione (GSH), were assessed. Additionally, the expression of genes related to apoptosis (p53) and autophagy (Beclin1, Atg7, P62) in the liver was evaluated. To validate the gene expression results, the protein expression levels of LC3 and p53 were also measured.</div></div><div><h3>Results</h3><div>Alcohol exposure elevated MDA levels while reducing SOD activity and GSH. Hydrolysate treatment restored antioxidant capacity by enhancing SOD and GSH and lowering MDA. Histology showed hepatic steatosis and reduced glycogen in group A, while groups P and AP exhibited significant improvement (p˂0.05). Additionally, hydrolysates inhibited alcohol-induced P53 upregulation and modulated autophagy-related genes (p˂0.05). Immunohistochemistry showed reduced P53 and increased LC3 in the AP group, indicating a shift from apoptosis to autophagy for cellular homeostasis.</div></div><div><h3>Conclusion</h3><div>These results suggest that protein hydrolysates derived from rainbow trout may have therapeutic potential as a dietary intervention for managing alcohol-induced liver injury, pending further validation.</div></div>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"44 ","pages":"Article 102238"},"PeriodicalIF":2.2000,"publicationDate":"2025-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Mitigating alcohol-induced liver oxidative stress and dysregulated autophagy with protein hydrolysates derived from rainbow trout by-products\",\"authors\":\"Fahimeh Hasani Zangbar , Ebrahim Najdegerami , Mojtaba Hadian , Ali Shalizar-Jalali\",\"doi\":\"10.1016/j.bbrep.2025.102238\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><h3>Background</h3><div>Chronic alcohol consumption causes irreversible liver damage. With 23 % waste from 29 million tons of annual production, rainbow trout is a valuable source of natural antioxidants. This study explores the hepatoprotective effects of rainbow trout protein hydrolysates in an alcohol-induced fatty liver disease (AFLD) rat model, focusing on autophagy, apoptosis, and oxidative stress pathways.</div></div><div><h3>Methods</h3><div>Twenty-four male rats were divided into four groups: Control (C), alcohol (A), protein hydrolysates (P), and alcohol + protein hydrolysates (AP). At the end of the experiment, liver tissue samples were collected for analysis. Oxidative stress markers, including malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione (GSH), were assessed. Additionally, the expression of genes related to apoptosis (p53) and autophagy (Beclin1, Atg7, P62) in the liver was evaluated. To validate the gene expression results, the protein expression levels of LC3 and p53 were also measured.</div></div><div><h3>Results</h3><div>Alcohol exposure elevated MDA levels while reducing SOD activity and GSH. Hydrolysate treatment restored antioxidant capacity by enhancing SOD and GSH and lowering MDA. Histology showed hepatic steatosis and reduced glycogen in group A, while groups P and AP exhibited significant improvement (p˂0.05). Additionally, hydrolysates inhibited alcohol-induced P53 upregulation and modulated autophagy-related genes (p˂0.05). Immunohistochemistry showed reduced P53 and increased LC3 in the AP group, indicating a shift from apoptosis to autophagy for cellular homeostasis.</div></div><div><h3>Conclusion</h3><div>These results suggest that protein hydrolysates derived from rainbow trout may have therapeutic potential as a dietary intervention for managing alcohol-induced liver injury, pending further validation.</div></div>\",\"PeriodicalId\":8771,\"journal\":{\"name\":\"Biochemistry and Biophysics Reports\",\"volume\":\"44 \",\"pages\":\"Article 102238\"},\"PeriodicalIF\":2.2000,\"publicationDate\":\"2025-09-29\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Biochemistry and Biophysics Reports\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S2405580825003255\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"BIOCHEMISTRY & MOLECULAR BIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Biochemistry and Biophysics Reports","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S2405580825003255","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
Mitigating alcohol-induced liver oxidative stress and dysregulated autophagy with protein hydrolysates derived from rainbow trout by-products
Background
Chronic alcohol consumption causes irreversible liver damage. With 23 % waste from 29 million tons of annual production, rainbow trout is a valuable source of natural antioxidants. This study explores the hepatoprotective effects of rainbow trout protein hydrolysates in an alcohol-induced fatty liver disease (AFLD) rat model, focusing on autophagy, apoptosis, and oxidative stress pathways.
Methods
Twenty-four male rats were divided into four groups: Control (C), alcohol (A), protein hydrolysates (P), and alcohol + protein hydrolysates (AP). At the end of the experiment, liver tissue samples were collected for analysis. Oxidative stress markers, including malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione (GSH), were assessed. Additionally, the expression of genes related to apoptosis (p53) and autophagy (Beclin1, Atg7, P62) in the liver was evaluated. To validate the gene expression results, the protein expression levels of LC3 and p53 were also measured.
Results
Alcohol exposure elevated MDA levels while reducing SOD activity and GSH. Hydrolysate treatment restored antioxidant capacity by enhancing SOD and GSH and lowering MDA. Histology showed hepatic steatosis and reduced glycogen in group A, while groups P and AP exhibited significant improvement (p˂0.05). Additionally, hydrolysates inhibited alcohol-induced P53 upregulation and modulated autophagy-related genes (p˂0.05). Immunohistochemistry showed reduced P53 and increased LC3 in the AP group, indicating a shift from apoptosis to autophagy for cellular homeostasis.
Conclusion
These results suggest that protein hydrolysates derived from rainbow trout may have therapeutic potential as a dietary intervention for managing alcohol-induced liver injury, pending further validation.
期刊介绍:
Open access, online only, peer-reviewed international journal in the Life Sciences, established in 2014 Biochemistry and Biophysics Reports (BB Reports) publishes original research in all aspects of Biochemistry, Biophysics and related areas like Molecular and Cell Biology. BB Reports welcomes solid though more preliminary, descriptive and small scale results if they have the potential to stimulate and/or contribute to future research, leading to new insights or hypothesis. Primary criteria for acceptance is that the work is original, scientifically and technically sound and provides valuable knowledge to life sciences research. We strongly believe all results deserve to be published and documented for the advancement of science. BB Reports specifically appreciates receiving reports on: Negative results, Replication studies, Reanalysis of previous datasets.