Hepatoprotective effect of Alhagi sparsifolia against Alcoholic Liver injury in mice

Kuerbanjiang Maimaitimin,Mikeremu Shayibuzhati,Zhihui Jiang,Aili Aierken,Xiaoying Zhang

doi:10.1590/s2175-97902018000317732

Abstract

Overconsumption of alcohol leads to alcoholic liver disease (ALD). Natural compounds have been investigated previously for their hepatoprotective activities against liver injury. This study investigated the protective effect of Alhagi sparsifolia on ALD. Alcohol was administered to mice for three consecutive days; either alone or in combination with Alhagi sparsifolia extract (150, 300, 600 mg/kg). Serum aspartate aminotransferase and alanine transaminase as biomarkers of liver injury, the content of malonaldehyde, hydrogen peroxide (H2O2) and glutathione which indicated the redox status of liver and the antioxidant enzyme activity of super oxide dismutase were detected, respectively. Moreover, the expression of protein cytochrome P450 2E1 (CYP2E1) the key enzyme of alcohol metabolism, and also tested by western blot experiment. Subsequently, the mRNA levels of inflammatory factors including TNF- α and TLR4 was determined real-time PCR. Results showed that Alhagi sparsifolia significantly alleviated alcohol-induced liver injury by reducing serum ALT and AST, inhibiting MDA and H2O2 content, increasing SOD, and GSH level in the liver (P< 0.05). In addition, the Alhagi sparsifolia treatment inhibited the expression of CYP2E1 (P< 0.05). The results suggest that Alhagi sparsifolia could be a promising natural substance for ameliorating acute alcohol-induced oxidative stress and hepatic injury.

Highlights

Alcoholic liver disease (ALD) is one of the most common causes of liver injury, accounting for 3.8% of all global deaths and 4.6% of global disability-adjusted life-years attributable to alcohol (Rehmet al., 2009)
Among the CYP450 family, cytochrome 2E1 (CYP2E1) has been identified as a key microsomal enzyme in alcoholic liver injury, since it is highly inducible with high catalytic activity against alcohol, which catalyzes the oxidation of exogenous and endogenous compounds, and it plays a significant role in the metabolism of alcohol by the liver
Alcohol overdose markedly increased mRNA expressions level including TLR4 and tumor necrosis factor-α (TNF-α) (Figure 3), which decreased significantly in the group pre-treated with Alhagi sparsifolia in a dose-dependent manner, suggesting that Alhagi sparsifolia mediated its anti-inflammatory effect at the transcriptional level

Summary

Introduction

Alcoholic liver disease (ALD) is one of the most common causes of liver injury, accounting for 3.8% of all global deaths and 4.6% of global disability-adjusted life-years attributable to alcohol (Rehmet al., 2009). The precise mechanisms and factors responsible for liver injury are not completely understood, many pathways have been suggested in which oxidative stress plays a key role in alcohol-induced liver injury (Cederbaum, 2001; Arteel, 2003). Among the CYP450 family, cytochrome 2E1 (CYP2E1) has been identified as a key microsomal enzyme in alcoholic liver injury, since it is highly inducible with high catalytic activity against alcohol, which catalyzes the oxidation of exogenous and endogenous compounds, and it plays a significant role in the metabolism of alcohol by the liver. It is relevant to the development of ALD caused by the generation of alcohol-induced reactive oxygen species (ROS) (Wang, 2010), which leads to lipid peroxidation in liver cells, and changes of alcohol metabolizing enzymes (Charles et al, 1985). Alcohol use results in the production of inflammatory cytokines such as

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