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

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.