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Original Research

Open Access

Esculentoside A inhibits ethyl alcohol-induced lipid accumulation and oxidative stress in hepatocytes by activating the AMPK pathway

  • Zhipeng Tang1
  • Peng Zhang2
  • Lu Li1
  • Yang Guo1
  • Yan You1
  • Yong Liao1,*,

1Department of Pharmacy, Affiliated Renhe Hospital of China Three Gorges University, 443001 Yichang, Hubei, China

2Department of Stomatology, Affiliated Renhe Hospital of China Three Gorges University, 443001 Yichang, Hubei, China

DOI: 10.22514/jomh.2023.119 Vol.19,Issue 11,November 2023 pp.82-89

Submitted: 13 July 2023 Accepted: 12 October 2023

Published: 30 November 2023

*Corresponding Author(s): Yong Liao E-mail: ly28368@163.com

Abstract

Alcoholic fatty liver disease (AFLD) is a liver illness resulting from excessive alcohol consumption. Esculentoside A (EsA) possesses various properties, including antioxidative and anti-inflammatory capabilities, but its role and mechanism in AFLD have remained unclear. In this study, we aimed to elucidate the functions of EsA in AFLD. We utilized ethyl alcohol-induced Alpha Mouse 12 (AML-12) cells as a model to mimic AFLD conditions. Cell viability was evaluated utilizing the Cell Counting Kit-8 assay. Lipid accumulation was quantified via Oil Red O staining. The expression levels of key genes associated with lipid accumulation were determined using quantitative reverse transcriptase polymerase chain reaction (qRT-PCR), and the contents of triglycerides (TG), aspartate aminotransferase (AST), alanine aminotransferase (ALT), reactive oxygen species (ROS) and superoxide dismutase (SOD) activity were quantified using commercially available assay kits. Additionally, western blot was performed to determine the levels of p-AMP-activated protein kinase (AMPK) Thr172/AMPK and peroxisome proliferator-activated receptor-alpha (PPARα). Our findings demonstrate that EsA effectively mitigated the damage induced by ethanol (EtOH) in AML-12 cells. Notably, EsA exhibited significant inhibitory effects on EtOH-induced lipid accumulation and oxidative stress in AML-12 cells. Importantly, our data suggest a potential connection between EsA-mediated effects and the activation of the AMPK pathway in EtOH-induced damage to AML-12 cells. In conclusion, EsA demonstrates promise in attenuating ethyl alcohol-induced lipid accumulation and oxidative stress in hepatocytes, likely through the activation of the AMPK pathway.


Keywords

Esculentoside A; Alcoholic fatty liver disease; Lipid accumulation; Oxidative stress; AMPK pathway


Cite and Share

Zhipeng Tang,Peng Zhang,Lu Li,Yang Guo,Yan You,Yong Liao. Esculentoside A inhibits ethyl alcohol-induced lipid accumulation and oxidative stress in hepatocytes by activating the AMPK pathway. Journal of Men's Health. 2023. 19(11);82-89.

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