Literature DB >> 32051738

Tartary buckwheat extract alleviates alcohol-induced acute and chronic liver injuries through the inhibition of oxidative stress and mitochondrial cell death pathway.

Qiang Yang1, Chengliang Luo2,3, Xinmu Zhang2, Yuancai Liu1, Zufeng Wang2,3, Piergiacomo Cacciamani2, Jiao Shi1, Yongchun Cui2, Chunling Wang2, Bharati Sinha2, Bin Peng2, Guoqiang Tong1, Gapika Das2, Elisha Shah2, Yuan Gao4, Wei Li2, Yanyang Tu2, Dongyang Qian4, Khalid Shah2, Mohammed Akbar5, Shuanhu Zhou4, Byoung-Joon Song6, Xin Wang2.   

Abstract

Alcohol use disorder (AUD) is an enormous public health problem that poses significant social, medical, and economic burdens. Under AUD, the liver is one of the most adversely affected organs. As current therapies and protective drugs for AUD-mediated liver injury are very limited, the prevention and therapy of alcoholic liver disease are urgently needed. The present study aims to investigate the beneficial effects of tartary buckwheat extract (TBE), the important component of Maopu tartary buckwheat liquor, on both alcoholic-induced acute and chronic liver injuries. We show that the TBE administration, similar to curcumin, significantly reduces the elevated serum aspartate aminotransferase and alanine aminotransferase levels, improves liver index, alleviates the elevated contents of hepatic malondialdehye, and restores the decreased contents of hepatic glutathione both in acute and chronic liver injuries in alcohol-exposed rats. Furthermore, histopathological analyses show that a medium dose of TBE (16.70 ml/kg body weight) alleviates hepatocyte morphology changes in both acute and chronic alcohol exposure models. We also show the protective effects of TBE on the cell death rates of alcohol-exposed primary cultured hepatocytes, HepG2 hepatoma, and Huh 7 hepatoma cells. Furthermore, we demonstrate that TBE exerts hepatoprotection partly through inhibiting the mitochondrial cell death pathway by reducing cytochrome c release, caspase-9 and -3 activities, and the number of TUNEL-positive cells. These effects of TBE were accompanied by enhanced levels of Bcl-2 and Bcl-xL and autophagic cell death pathway by reducing Beclin-1 expression, as well as through promoting its anti-oxidant capacity by suppressing reactive oxygen species production. This study demonstrates, for the first time, the protective effect of TBE against alcohol-induced acute and chronic liver injury in vivo and in vitro. Given the dietary nature of tartary buckwheat, pueraria, lycium barbarum, and hawthorn, the oral intake of TBE or liquor contained TBE, e.g., Maopu Tartary buckwheat liquor, compared with pure liquor consumption alone, may have the potential to alleviate alcoholic-induced liver injuries. AJTR
Copyright © 2020.

Entities:  

Keywords:  Tartary buckwheat extract (TBE); alcoholic liver injuries; mitochondrial cell death; oxidative stress

Year:  2020        PMID: 32051738      PMCID: PMC7013218     

Source DB:  PubMed          Journal:  Am J Transl Res        ISSN: 1943-8141            Impact factor:   4.060


  60 in total

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Review 7.  Medications for alcohol use disorders: An overview.

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8.  Effect of dietary Tartary buckwheat extract supplementation on growth performance, meat quality and antioxidant activity in ewe lambs.

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Review 9.  Acute-on-chronic liver failure: terminology, mechanisms and management.

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10.  The Effects of Buckwheat Leaf and Flower Extracts on Antioxidant Status in Mouse Organs.

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Review 3.  Protective Mechanism of Edible Food Plants against Alcoholic Liver Disease with Special Mention to Polyphenolic Compounds.

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