Abstract

It has been reported that barley leaves possess beneficial properties such as antioxidant, hypolipidemic, antidepressant, and antidiabetic. Interestingly, barley sprouts contain a high content of saponarin, which showed both anti-inflammatory and antioxidant activities. In this study, we evaluated the effect of barley sprouts on alcohol-induced liver injury mediated by inflammation and oxidative stress. Raw barley sprouts were extracted, and quantitative and qualitative analyses of its components were performed. The mice were fed a liquid alcohol diet with or without barley sprouts for four weeks. Lipopolysaccharide (LPS)-stimulated RAW 264.7 cells were used to study the effect of barley sprouts on inflammation. Alcohol intake for four weeks caused liver injury, evidenced by an increase in serum alanine aminotransferase and aspartate aminotransferase activities and tumor necrosis factor (TNF)-α levels. The accumulation of lipid in the liver was also significantly induced, whereas the glutathione (GSH) level was reduced. Moreover, the inflammation-related gene expression was dramatically increased. All these alcohol-induced changes were effectively prevented by barley sprouts treatment. In particular, pretreatment with barley sprouts significantly blocked inducible nitric oxide synthase (iNOS) and cyclooxygenase (COX)-2 expression in LPS-stimulated RAW 264.7. This study suggests that the protective effect of barley sprouts against alcohol-induced liver injury is potentially attributable to its inhibition of the inflammatory response induced by alcohol.

Highlights

  • Fatty liver or hepatic steatosis is defined as the accumulation of triglycerides in the liver, leading to more than 5% of the hepatic cells containing either micro- or macrovesicular lipid droplets

  • We hypothesized that the extract of barley ameliorate chronic alcohol-induced liver injury mediated by an inflammatory responsebyand, sprouts could have the potential to ameliorate chronic alcohol‐induced liver injury mediated an we investigated our hypothesis in this study

  • For saponarin according to athat concentration‐dependent electrospray spectrometer method

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Summary

Introduction

Fatty liver or hepatic steatosis is defined as the accumulation of triglycerides in the liver, leading to more than 5% of the hepatic cells containing either micro- or macrovesicular lipid droplets. Nutrients 2016, 8, 440 from simple steatosis to cirrhosis It is highly prevalent and holds a high rank in the causes of death worldwide, preventive and therapeutic approaches have yet to be discovered [1,2]. The liver cells have various sources of reactive oxygen species (ROS) which are activated by chronic alcohol consumption, leading to an increase in the generation of oxidants [4]. It is highly prevalent and holds a high rank in the causes increases thefrom permeability of intestinal mucosa and sensitizes Kupffer cells to activation by endotoxins of death worldwide, preventive and therapeutic approaches have yet to be discovered [1,2]

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