Hepatoprotective effect of gastrodin against alcohol-induced liver injury in mice
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ORIGINAL ARTICLE
Hepatoprotective effect of gastrodin against alcohol-induced liver injury in mice Xin-Xin Li 1 & Zhi-Hui Jiang 1 & Bo Zhou 1 & Chen Chen 1 & Xiao-Ying Zhang 1,2,3 Received: 23 July 2017 / Accepted: 2 September 2018 # University of Navarra 2018
Abstract Alcoholic liver disease (ALD) is a common and serious threat to human health worldwide. In this study, the hepatoprotective effect of gastrodin against alcohol-induced liver injury in mice was examined. Mice with alcohol-induced hepatotoxicity were treated intragastrically with gastrodin (50, 80, or 100 mg/kg). The mice treated with gastrodin experienced better outcomes than those who received only one dose of alcohol (50%, 10 mL/kg b.w.). Gastrodin treatment reduced the activities of serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST), decreased hepatic malondialdehyde (MDA) content, and increased hepatic superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase (CAT) activities in a dose-dependent manner. Gastrodin also alleviated histopathological changes induced by alcohol. Gastrodin protected against alcohol-induced increases in expression levels of the cytochrome P450 2E1 (CYP2E1) and mRNA levels of chemokine (C-X-C motif) ligand 1 (CXCL-1), interferon-γ (IFN-γ), interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-α), vascular cell adhesion molecule 1 (VCAM-1), nuclear factor-kappa B (NF-κB), Toll-like receptor 4 (TLR-4), and activator of transcription 3 (STAT-3). Moreover, gastrodin-increased nuclear transcription factor 2 (Nrf2) translocates to the nucleus and enhanced the activity of anti-oxidant enzymes, and could thereby ameliorate alcohol-induced liver injury in mice. This study demonstrated that gastrodin may be an effective therapeutic agent against alcohol-induced liver injury. Keywords Gastrodin . Alcohol . Hepatic injury . Anti-oxidant . Inflammation
Introduction Alcoholic liver disease (ALD), which refers to changes within the liver caused by excessive alcohol, is a common disease worldwide [4]. ALD is caused by over-production of reactive oxygen species (ROS), lipid peroxidation injury, cytokine * Chen Chen [email protected] * Xiao-Ying Zhang [email protected]; [email protected] 1
Chinese-German Joint Laboratory for Natural Product Research, College of Biological Science and Engineering, Qingling-Bashan Mountains Bioresources Comprehensive Development C.I.C, Shaanxi University of Technology, East on the 1st Ring Road, Hanzhong 723000, Shaanxi Province, China
2
College of Veterinary Medicine, Northwest A&F University (North Campus), Xinong Rd. 22, Post Box 19, Yangling 712100, Shaanxi Province, China
3
Centre of Molecular and Environmental Biology, Department of Biology, University of Minho, Campus de Gualtar, 4710-057 Braga, Portugal
damage, and inflammation [27]. In recent years, the incidence of ALD has increased, posing a serious threat to human health [4]. Thus, research on drugs that are effective in interfering with the course of ALD is vital. ALD has a complex pathogene
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