L. Mitigates Hyperlipidemia-Induced Nonalcoholic Fatty Liver Disease in Experimental Rats: Future Pharmaceuticals.

Nonalcoholic fatty liver disease (NAFLD) associated with hyperlipidemia is a prevalent metabolic disorder, often triggered by high-fat diets (HFDs) in animal models. L. (AGs), rich in bioactive compounds, offers potential antioxidant and lipid-lowering benefits, making it a candidate for natural liver protection. This study evaluated the protective role of L. against hyperlipidemia-induced NAFLD in rats. Thirty male Wistar rats (150 ± 20 g, 10 weeks old) were split into five groups ( = 6 each). A control group received 0.25 mL 0.1% DMSO orally. Four HFD-fed groups included one with only DMSO (0.25 mL) and three supplemented with AG solution (0.25 mL) at 100, 200, or 500 mg/kg body weight. Treatments were given daily via gavage for two months. AGs' nutritional profile, serum lipids, liver function, and liver histology were analyzed. AGs contain 21.3% protein, 1.1% fat, 15% fiber, moderate vitamins (ascorbic acid, B-complex), and minerals (high potassium, calcium; low magnesium, phosphorus, sodium). AG-treated rats weighed less than the HFD controls. Unlike the control group (normal lipids, liver function, no steatosis), the HFD rats showed severe hyperlipidemia, liver dysfunction, and steatosis with fat changes. The AG groups exhibited dose-dependent improvements in lipids and liver function; the 200 mg/kg group had reduced fatty changes, and the 500 mg/kg group showed minimal hepatocyte fat. L. reduces hyperlipidemia and NAFLD progression in HFD-fed rats, which suggests its potential as a natural liver-protective agent.