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牡蛎肽对酒精性肝病小鼠的保护作用。

Hepatoprotective Effect of Oyster Peptide on Alcohol-Induced Liver Disease in Mice.

机构信息

CAS and Shandong Province Key Laboratory of Experimental Marine Biology, Center for Ocean Mega-Science, Institute of Oceanology, Chinese Academy of Sciences, Qingdao 266071, China.

Laboratory for Marine Drugs and Bioproducts, Pilot National Laboratory for Marine Science and Technology (Qingdao), No. 1 Wenhai Road, Qingdao 266237, China.

出版信息

Int J Mol Sci. 2022 Jul 22;23(15):8081. doi: 10.3390/ijms23158081.

Abstract

Alcohol-induced liver disease (ALD) has become one of the major global health problems, and the aim of this study was to investigate the characterization of the structure as well as the hepatoprotective effect and mechanism of oyster peptide (OP, MW < 3500 Da) on ALD in a mouse model. The results demonstrate that ethanol administration could increase the activities of aspartate aminotransferase (AST), alanine transaminase (ALT), γ-Glutamyl transferase (GGT), reactive oxygen species (ROS), malondialdehyde (MDA), and triglycerides (TG), as well as increase the interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor (TNF-α) levels (p < 0.01), and reduce the activity of superoxide dismutase (SOD) and the concentration of glutathione (GSH). Those changes were significantly reversed by the application of different doses of OP. Furthermore, the mRNA expressions of nuclear factor elythroid 2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1), and quinone oxidoreductase1 (NQO1) were significantly up-regulated in OP groups, and the mRNA expressions of nuclear factor kappa-light chain enhancer of B cells (NF-κB), TNF-α, and IL-6 were markedly reduced in OP groups compared to that of the model group. Thus, OP had a significant protective effect on ALD through the enhancement of the in vivo antioxidant ability and the inhibition of the inflammatory response as possible mechanisms of action, which therefore suggests that OP might be useful as a natural source to protect the liver from alcohol damage.

摘要

酒精性肝病 (ALD) 已成为全球主要的健康问题之一,本研究旨在探讨牡蛎肽 (OP,MW < 3500 Da) 对酒精性肝病小鼠模型的结构特征、保肝作用及其机制。结果表明,乙醇处理可使天冬氨酸转氨酶 (AST)、丙氨酸转氨酶 (ALT)、γ-谷氨酰转移酶 (GGT)、活性氧 (ROS)、丙二醛 (MDA) 和甘油三酯 (TG) 活性升高,白介素-1β (IL-1β)、白介素-6 (IL-6) 和肿瘤坏死因子 (TNF-α) 水平升高 (p < 0.01),超氧化物歧化酶 (SOD) 活性和谷胱甘肽 (GSH) 浓度降低。不同剂量的 OP 可显著逆转这些变化。此外,OP 组核因子红细胞 2 相关因子 2 (Nrf2)、血红素加氧酶-1 (HO-1) 和醌氧化还原酶 1 (NQO1) 的 mRNA 表达明显上调,而 NF-κB、TNF-α 和 IL-6 的 mRNA 表达明显下调。因此,OP 通过增强体内抗氧化能力和抑制炎症反应对 ALD 具有显著的保护作用,这可能是其作用机制之一,提示 OP 可能作为一种天然来源,用于保护肝脏免受酒精损伤。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/790d/9332721/afd0928b65d7/ijms-23-08081-g001.jpg

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