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Biochimie. 2018 Jul;150:131-138. doi: 10.1016/j.biochi.2018.05.008. Epub 2018 May 19.

Chlorogenic acid ameliorates alcohol-induced liver injuries through scavenging reactive oxygen species.

Author information

1
School of Life Sciences, BK21 Plus KNU Creative BioResearch Group, College of Natural Sciences, Kyungpook National University, Taegu, Republic of Korea.
2
School of Human Environmental Sciences, University of Arkansas, Fayetteville, AR, USA.
3
Department of Food and Biotechnology, Korea University, Sejong, Republic of Korea.
4
School of Life Sciences, BK21 Plus KNU Creative BioResearch Group, College of Natural Sciences, Kyungpook National University, Taegu, Republic of Korea. Electronic address: parkjw@knu.ac.kr.

Abstract

The key role of oxidative stress in alcoholic liver disease (ALD) has been established by the large body of evidence from previous studies. Excessive consumption of ethanol induces the production of a variety of reactive oxygen species (ROS) in the liver, such as superoxide, H2O2, and hydroxyl radical. These products activate oxidant-sensitive signaling cascades and modulators of apoptosis. Because ROS accumulation is closely related to ALD, a number of studies have investigated the benefits of antioxidants. Recent studies demonstrated that polyphenol chlorogenic acid (CGA) has antioxidant properties and health benefits, such as reduction of relative risk of cardiovascular diseases and hepatoprotective effects against acetaminophen toxicity. However, the protective effects of CGA against ALD have not been studied in detail. We hypothesize that CGA plays a role in preventing ALD through its antioxidant properties. In this study, we investigated the protective effects of CGA against liver injuries in vivo. Reduced alcohol-induced-steatosis, apoptotic cell death, and fibrosis due to reduced levels of oxidative stress were observed. These findings suggest that CGA treatment can be an effective approach to attenuate ALD through the suppression of oxidative stress.

KEYWORDS:

ALD; Alcohol; Apoptosis; Chlorogenic acid; ROS

PMID:
29787793
DOI:
10.1016/j.biochi.2018.05.008
[Indexed for MEDLINE]

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