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S-腺苷甲硫氨酸及其与牛磺酸和/或甜菜碱的组合对乙醇诱导的急性肝毒性中谷胱甘肽稳态的影响。

Effects of S-Adenosylmethionine and Its Combinations With Taurine and/or Betaine on Glutathione Homeostasis in Ethanol-induced Acute Hepatotoxicity.

作者信息

Lee Seo Yeon, Ko Kwang Suk

机构信息

Department of Nutritional Science and Food Management, Ewha Womans University, Seoul, Korea.

出版信息

J Cancer Prev. 2016 Sep;21(3):164-172. doi: 10.15430/JCP.2016.21.3.164. Epub 2016 Sep 30.

DOI:10.15430/JCP.2016.21.3.164
PMID:27722142
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5051590/
Abstract

BACKGROUND

Exposure to ethanol abuse and severe oxidative stress are risk factors for hepatocarcinoma. The aim of this study was to evaluate the effects of S-adenosylmethionine (SAMe) and its combinations with taurine and/or betaine on the level of glutathione (GSH), a powerful antioxidant in the liver, in acute hepatotoxicity induced by ethanol.

METHODS

To examine the effects of SAMe and its combinations with taurine and/or betaine on ethanol-induced hepatotoxicity, AML12 cells and C57BL/6 mice were pretreated with SAMe, taurine, and/or betaine, followed by ethanol challenge. Cell viability was detected with an MTT assay. GSH concentration and mRNA levels of GSH synthetic enzymes were measured using GSH reductase and quantitative real-time reverse transcriptase-PCR. Alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities were measured with commercially available kits.

RESULTS

Pretreatment of SAMe, with or without taurine and/or betaine, attenuated decreases in GSH levels and mRNA expression of the catalytic subunit of glutamate-cysteine ligase (GCL), the rate-limiting enzyme for GSH synthesis, in ethanol-treated cells and mice. mRNA levels of the modifier subunit of GCL and glutathione synthetase were increased in mice treated with SAMe combinations. SAMe, taurine, and/or betaine pretreatment restored serum ALT and AST levels to control levels in the ethanol-treated group.

CONCLUSIONS

Combinations of SAMe with taurine and/or betaine have a hepatoprotective effect against ethanol-induced liver injury by maintaining GSH homeostasis.

摘要

背景

乙醇滥用和严重氧化应激是肝癌的危险因素。本研究旨在评估S-腺苷甲硫氨酸（SAMe）及其与牛磺酸和/或甜菜碱的组合对乙醇诱导的急性肝毒性中肝脏强效抗氧化剂谷胱甘肽（GSH）水平的影响。

方法

为了检测SAMe及其与牛磺酸和/或甜菜碱的组合对乙醇诱导的肝毒性的影响，AML12细胞和C57BL/6小鼠先用SAMe、牛磺酸和/或甜菜碱预处理，然后进行乙醇刺激。用MTT法检测细胞活力。使用谷胱甘肽还原酶和定量实时逆转录聚合酶链反应测量GSH浓度和GSH合成酶的mRNA水平。用市售试剂盒测量丙氨酸转氨酶（ALT）和天冬氨酸转氨酶（AST）活性。

结果

SAMe预处理，无论有无牛磺酸和/或甜菜碱，均可减轻乙醇处理的细胞和小鼠中GSH水平的降低以及谷氨酸-半胱氨酸连接酶（GCL）催化亚基的mRNA表达降低，GCL是GSH合成的限速酶。用SAMe组合处理的小鼠中，GCL调节亚基和谷胱甘肽合成酶的mRNA水平升高。SAMe、牛磺酸和/或甜菜碱预处理可使乙醇处理组的血清ALT和AST水平恢复至对照水平。

结论

SAMe与牛磺酸和/或甜菜碱的组合通过维持GSH稳态对乙醇诱导的肝损伤具有肝保护作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2497/5051590/bb34f3d536b1/jcp-21-164f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2497/5051590/4d5856043c0a/jcp-21-164f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2497/5051590/e1c2ca480627/jcp-21-164f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2497/5051590/8607671a24fb/jcp-21-164f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2497/5051590/bb34f3d536b1/jcp-21-164f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2497/5051590/4d5856043c0a/jcp-21-164f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2497/5051590/e1c2ca480627/jcp-21-164f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2497/5051590/8607671a24fb/jcp-21-164f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2497/5051590/bb34f3d536b1/jcp-21-164f4.jpg

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