Abstract
Lipid accumulation is the most vital risk factor for inducing nonalcoholic fatty liver disease (NAFLD) and metabolic syndrome. Thus, the development of novel drugs is urgently needed to control obesity related diseases.
Here, we investigated the protective role of Lavatera critica (LC), a green vegetable, in male C57BL/6J mice fed with high fat (HF) diet for 10 weeks to induce hepatic lipid accumulation and oxidative cellular damage.
After oral administration of chloroform (CFLC), ethyl acetate (EFLC), or methanol (MFLC) fractions of Lavatera critica to the HF group, EALC alone significantly reduced the activities of hepatic markers such as alanine aminotransferase (ALT) and aspartate aminotransferase (AST); moreover, the results showed that 50 mg/kg dose has the maximum activity. Thus, this active dose of EFLC was used for further analysis. Moreover, EFLC reduced the level of hepatic triglycerides (TG), total cholesterol (TC), free fatty acids (FFA), and prevented further increase in the body weight. Intriguingly, EFLC treatment also reversed the mRNA expression of fatty acid oxidative genes, such as peroxisome proliferator activated receptor-α (PPAR-α), carnitine palmitoyltransferase-1 (CPT-1), and acetyl-CoA carboxylase (ACO), and fatty acid synthesis genes such as fatty acid synthase (FAS), sterol-regulatory-element-binding protein-1c (SREBP-1c), and acetyl-CoA carboxylase (ACC). Furthermore, EFLC treatment also decreased the production of oxidative stress biomarkers, such as conjugated diene (CD), thiobarbituric acid reactive substances (TBARS), and lipid hydroperoxide (LOOH), and significantly enhanced the level of enzymatic antioxidants, such as glutathione peroxidase (GPx), superoxide dismutase (SOD), and catalase (CAT), as well as non-enzymatic antioxidants, such as reduced glutathione (GSH), vitamin C, and vitamin E in the liver.
Taken together, we conclude that EFLC has a protective effect against HF diet induced hepatic lipid accumulation and oxidative cellular damage through the regulation of lipogenesis and lipolysis genes.