Astragaloside alleviates alcoholic fatty liver disease by suppressing oxidative stress

Alcoholic fatty liver disease (AFLD) is the most common liver disease and can progress to fatal liver cirrhosis and carcinoma, affecting millions of patients worldwide. The functions of astragaloside on the cardiovascular system have been elucidated. However, its role in AFLD is unclear. Ethanol‐tre...

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Bibliographic Details
Published in:	The Kaohsiung journal of medical sciences 2021-08, Vol.37 (8), p.718-729
Main Authors:	Jiang, Zhi‐Bin, Gao, Jie, Chai, Yi‐Hui, Li, Wen, Luo, Yun‐Feng, Chen, Yun‐Zhi
Format:	Article
Language:	eng
Subjects:	Alcohol use alcoholic fatty liver disease Animals Apoptosis Apoptosis - drug effects astragaloside B cells Bilirubin Bioengineering Biotechnology industry Cell culture Cell Line Chinese medicine Development and progression Disease Models, Animal Ethanol Fatty liver Fatty Liver, Alcoholic - metabolism Fatty Liver, Alcoholic - prevention & control Ferritin Inflammation Inflammation - metabolism Inflammation - prevention & control lipid accumulation Lipid Metabolism - drug effects Lipids Liver cirrhosis Liver diseases Liver Function Tests Male Mitochondrial DNA NF-kappa B - metabolism Oxidative stress Oxidative Stress - drug effects Rats Rats, Sprague-Dawley Reactive Oxygen Species - metabolism Saponins - pharmacology Scientific equipment and supplies industry Signal Transduction - drug effects Superoxide Triglycerides Triterpenes - pharmacology
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Summary:	Alcoholic fatty liver disease (AFLD) is the most common liver disease and can progress to fatal liver cirrhosis and carcinoma, affecting millions of patients worldwide. The functions of astragaloside on the cardiovascular system have been elucidated. However, its role in AFLD is unclear. Ethanol‐treated AML‐12 cells were used as a cell model of alcoholic fatty liver. Real‐time quantitative reverse transcription‐PCR and Western blotting detected genes and proteins expressions. Reactive oxygen species (ROS), triglyceride, total cholesterol, low‐density lipoprotein, albumin, ferritin, bilirubin, superoxide dismutase, aspartate aminotransferase (AST), and alanine aminotransferase (ALT) were examined using commercial kits. Lipid accumulation was assessed by Oil red O staining. MTT and flow cytometry measured cell viability and apoptosis. JC‐1 was used to analyze mitochondrial membrane potential. A rat model of AFLD was established by treating rats with ethanol. Astragaloside suppressed ethanol‐induced lipid accumulation, oxidative stress, and the production of AST and ALT in AML‐12 cells. Ethanol induced TNF‐α and reduced IL‐10 expression, which were reversed by astragaloside. Ethanol promoted Bax expression and cytochrome C release and inhibited Bcl‐2 and ATP expression. Astragaloside hampered these apoptosis effects in AML‐12 cells. Impaired mitochondrial membrane potential was recovered by astragaloside. However, all these astragaloside‐mediated beneficial effects were abolished by the ROS inducer pyocyanin. Ethanol‐induced activation of NF‐κB signaling was suppressed by astragaloside in vitro and in vivo, suggesting that astragaloside inhibited oxidative stress by suppressing the activation of NF‐κB signaling, thus improving liver function and alleviating AFLD in rats. Our study elucidates the pharmacological mechanism of astragaloside and provides potential therapeutic strategies for AFLD.
ISSN:	1607-551X 2410-8650