Supplementation of oat (Avena sativa L.) extract abates alcohol-induced acute liver injury in a mouse model

Nutr Res. 2018 Jun;54:80-92. doi: 10.1016/j.nutres.2018.04.002. Epub 2018 Apr 6.


Dietary supplementation of oats has been associated with reduced risk of cardiovascular disease, diabetes, and gastrointestinal disorders. The role of oat extract as prophylactic in treating acute liver injury is not thoroughly established. We, therefore, hypothesized that oat extract would exert protective effect against alcohol-induced acute liver injury in a mouse model. To test this hypothesis, male C57BL/6 mice were pretreated with phenolic-enriched ethyl acetate (EA) fraction of oats (prepared by fractionating aqueous ethanolic extract with solvents of increasing polarity) at dosages of 125 and 250 mg kg-1 d-1 for 12 consecutive days. Acute liver injury was induced by administering 5 doses of 50% ethanol intragastrically (10 g/kg body weight) to mice at an interval of 12 hours. The alcohol-induced liver injury was evaluated by measuring serum levels of alanine aminotransferase, aspartate aminotransferase, lactate dehydrogenase, antioxidant parameters, mitochondrial function, and histology of liver tissue. Our results demonstrated that pretreatment with EA fraction at 250 mg kg-1 d-1 significantly (P < .001 for aspartate aminotransferase, alanine aminotransferase, and thiobarbituric acid-reactive species and P < .01 for lactate dehydrogenase and nitrites) reduced the levels of liver injury markers and significantly (P < .001 for glutathione reductase and glutathione S-transferase; P < .01 for catalase, superoxide dismustase, and vitamin C; P < .05 for reduced glutathione and NAD(P)H quinone dehydrogenase 1) increased the levels of antioxidant defenses. Furthermore, EA-pretreated mice showed mechanistic inhibition of nuclear factor κB signaling pathway through decreased phosphorylation and degradation of IκBα. We conclude that phenolic-enriched EA fraction of oats has immense potential to serve as dietary intervention against alcohol-induced liver damage.

Keywords: Alcohol-induced acute liver injury; Antioxidants; Avenanthramides; Mitochondrial respiratory enzymes; Nuclear factor κB; Oat (Avena sativa L.) extract.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alanine Transaminase / blood
  • Animals
  • Antioxidants / metabolism
  • Antioxidants / pharmacology
  • Antioxidants / therapeutic use*
  • Aspartate Aminotransferases / blood
  • Avena / chemistry*
  • Catalase / metabolism
  • Chemical and Drug Induced Liver Injury / blood
  • Chemical and Drug Induced Liver Injury / metabolism
  • Chemical and Drug Induced Liver Injury / prevention & control*
  • Dietary Supplements
  • Ethanol / adverse effects*
  • Glutathione / metabolism
  • L-Lactate Dehydrogenase / blood
  • Liver / drug effects*
  • Liver / metabolism
  • Mice, Inbred C57BL
  • Phenols / pharmacology
  • Phenols / therapeutic use*
  • Phytotherapy*
  • Plant Extracts / pharmacology
  • Plant Extracts / therapeutic use
  • Superoxide Dismutase / metabolism
  • Thiobarbituric Acid Reactive Substances


  • Antioxidants
  • Phenols
  • Plant Extracts
  • Thiobarbituric Acid Reactive Substances
  • Ethanol
  • L-Lactate Dehydrogenase
  • Catalase
  • Superoxide Dismutase
  • Aspartate Aminotransferases
  • Alanine Transaminase
  • Glutathione