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

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.