Bacoside – A improves Non-Alcoholic Fatty Liver Disease in rats fed on a high fat diet

Abstract

The chronic illness known as nonalcoholic fatty liver disease (NAFLD) is linked to morbidity in the metabolic syndrome. NAFLD is a global issue that is primarily responsible for liver damage, which can result in the loss of liver cells. We looked into how rosuvastatin (RSV; 10 mg/kg) and Bacoside - A (Bac-A; 10 mg/kg) affected hepatic steatosis brought on by a high-fat diet (HFD). Male Sprague-Dawley rats were given Bac-A or RSV for four weeks after 16 weeks of HFD. We looked at the liver's apoptotic cell death, reactive oxygen species production, lipid content, metabolic parameters, and histological changes. In addition to the expression of the following significant molecules, we investigated the liver's metabolic parameters, function, fat content, histological changes, production of reactive oxygen species, and apoptotic cell death: transient receptor potential cation channel subfamily V member 1 (TRPV1) phosphorylation of sterol regulatory element binding protein (pSREBP-1c/SREBP-1 c), total and membrane glucose transporter 2 (GLUT2), 4-hydroxynonenal (4-HNE), and cleaved caspase-3. Significantly higher levels of morphological disarray, damage indicators, oxidative stress, lipid peroxidation, and apoptosis were linked to HFD-induced hepatic steatosis. However, RSV and Bac-A treatment decreased metabolic dysfunction and hepatic damage. Bac-A reduced oxidative stress and apoptotic cell death, enhanced insulin resistance, and controlled lipid accumulation. Consequently, Bac-A is a therapy strategy that shows promise for treating metabolic abnormalities in NAFLD patients.