酶解猪胎盘水解物对大鼠肝脏酒精代谢的激活作用。

Activation of hepatic alcohol metabolism by enzymatic porcine placenta hydrolysate in rats.

作者信息

Shin Jaeeun, Kim Ji-Sun, Jung Young Jae, Lee Yeonho, Yoo Haeyoung, Ju Seong Hun, Sim Daehyeon, Kim Yebean, Bae Gun Won, Yoon Sun Myung, Lee Sung-Joon

机构信息

Department of Biotechnology, Graduate School of Biotechnology, College of Life Science and Biotechnology, Korea University, Seoul, 02841 South Korea.

Unimed Pharmaceuticals Inc., UNIMED Bldg #69, Samjeon-ro, Songpa-gu, Seoul, 05567 South Korea.

出版信息

Food Sci Biotechnol. 2025 Feb 24;34(9):2025-2038. doi: 10.1007/s10068-025-01822-1. eCollection 2025 May.

DOI:10.1007/s10068-025-01822-1

PMID:40196334

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11972273/

Abstract

UNLABELLED

Alcohol consumption causes severe liver damage and oxidative stress. This study investigated the hepatoprotective effects of enzymatic porcine placenta hydrolysate (EPPH) in Sprague-Dawley rats under acute alcohol administration. EPPH significantly reduced plasma ethanol and acetaldehyde levels in a dose-dependent manner. Furthermore, EPPH decreased the hepatic levels of malondialdehyde and thiobarbituric acid reactive substances and suppressed mRNA expression. EPPH decreased the plasma alanine transaminase and aspartate transaminase levels and increased the hepatic NAD/NADH ratio. Hepatic transcriptome analysis revealed the significant regulation of key genes involved in inflammation, alcohol response, and apoptosis. Phosphokinase array analysis demonstrated that EPPH reduced phosphorylation of CASP9, BAX, TP53, and CHK2, thereby facilitating reactive oxygen species removal and suppressing apoptosis. Additionally, qPCR confirmed EPPH reduced and mRNA levels, while immunoblotting showed decreased phosphorylation of TP53 and CHK2. These findings suggest that EPPH improves hepatic alcohol metabolism and reduces alcohol-induced hepatotoxicity.

SUPPLEMENTARY INFORMATION

The online version contains supplementary material available at 10.1007/s10068-025-01822-1.

摘要

未标记

饮酒会导致严重的肝损伤和氧化应激。本研究调查了酶解猪胎盘水解物（EPPH）在急性酒精给药条件下对Sprague-Dawley大鼠的肝脏保护作用。EPPH以剂量依赖的方式显著降低了血浆乙醇和乙醛水平。此外，EPPH降低了肝脏中丙二醛和硫代巴比妥酸反应性物质的水平，并抑制了mRNA表达。EPPH降低了血浆丙氨酸转氨酶和天冬氨酸转氨酶水平，并提高了肝脏中NAD/NADH比值。肝脏转录组分析揭示了参与炎症、酒精反应和细胞凋亡的关键基因的显著调控。磷酸激酶阵列分析表明，EPPH降低了CASP9、BAX、TP53和CHK2的磷酸化，从而促进活性氧的清除并抑制细胞凋亡。此外，qPCR证实EPPH降低了和 mRNA水平，而免疫印迹显示TP53和CHK2的磷酸化减少。这些发现表明，EPPH改善了肝脏的酒精代谢并降低了酒精诱导的肝毒性。