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首页> 外文期刊>Alcohol >Lipoic acid protects gastric mucosa from ethanol-induced injury in rat through a mechanism involving aldehyde dehydrogenase 2 activation
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Lipoic acid protects gastric mucosa from ethanol-induced injury in rat through a mechanism involving aldehyde dehydrogenase 2 activation

机译：通过涉及醛脱氢酶2活化的机制，硫辛酸通过乙醇诱导的大鼠损伤免受乙醇诱导的损伤

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Numerous studies demonstrate that reactive aldehydes are highly toxic and aldehyde dehydrogenase 2 (ALDH2)-mediated detoxification of reactive aldehydes is thought as an endogenous protective mechanism against reactive aldehydes-induced cell injury. This study aims to explore whether lipoic acid, a potential ALDH2 activator, is able to protect gastric mucosa from ethanol-induced injury through a mechanism involving clearance of reactive aldehydes. The rats received 60% of acidified ethanol through intragastric administration and held for 1 h to establish a mucosal injury model. Lipoic acid (10 or 30 mg/kg) or Alda-1 (a positive control, 10 mg/kg) was given 45 min before the ethanol treatment. The gastric tissues were collected for analysis of gastric ulcer index, cellular apoptosis, 4-hydroxy-2-nonenal (4-HNE) and malondialdehyde (MDA) contents, and ALDH2 activity. The results showed that acute administration of ethanol led to an increase in gastric ulcer index, cellular apoptosis, 4-HNE and MDA contents concomitant with a decrease in ALDH2 activity; these phenomena were reversed by lipoic acid or Alda-1. The gastric protection of lipoic acid was attenuated in the presence of ALDH2 inhibitor. Based on these observations, we conclude that lipoic acid exerts the beneficial effects on ethanol-induced injury through a mechanism involving, at least in part, ALDH2 activation. As a dietary supplement or a medicine already in some countries, lipoic acid can be used to treat the ethanol - induced gastric mucosal injury. (C) 2016 Elsevier Inc. All rights reserved.
机译：许多研究表明，反应性醛是高毒性的，醛脱氢酶2（Aldh2）介导的反应性醛的解毒被认为是对反应性醛诱导的细胞损伤的内源保护机制。本研究旨在探讨硫辛酸是否能够通过涉及反应性醛的间隙的机制来保护胃粘膜免受乙醇诱导的损伤。大鼠通过胃内给药获得60％的酸化乙醇，并保持1小时以建立粘膜损伤模型。在乙醇处理前45分钟给出硫辛酸（10或30mg / kg）或Alda-1（阳性对照，10mg / kg）。收集胃组织以分析胃溃疡指数，细胞凋亡，4-羟基-2-壬比（4-HNE）和丙二醛（MDA）含量，以及Aldh2活性。结果表明，乙醇的急性施用导致胃溃疡指数，细胞凋亡，4-HNE和MDA含量的增加，随着ALDH2活性的降低而伴随着;这些现象由硫辛酸或ALDA-1逆转。在Ald2抑制剂存在下衰减硫辛酸的胃保护。基于这些观察结果，我们得出结论，硫辛酸通过涉及的机制施加对乙醇诱导的损伤的有益作用，该机制至少部分地是Aldh2活化。作为一些国家的膳食补充剂或药物，硫辛酸可用于治疗乙醇诱导的胃粘膜损伤。 （c）2016年Elsevier Inc.保留所有权利。

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