Ginsenoside F1 attenuates lipid accumulation and triglycerides content in 3T3-L1 adipocytes with the modulation of reactive oxygen species (ROS) production through PPAR-γ/JAK2 signaling responses

Abstract

Obesity is the severe health concern worldwide, causing a highest risk of mortality rate every year in different countries. During adipogenesis interactions with peroxisome proliferator-activated receptor gamma are mainly responsible for the development of obesity with regulation of the various transcription factors. It causes the increase of lipid accumulation, triglyceride content as well as reactive oxygen species production in adipocyte differentiation. Current drugs used as anti-obesity associated with several side effects. The present study was therefore conducted, to evaluate the protective and inhibitory effect of ginsenoside F1 from Panax ginseng on lipid accumulation and reactive oxygen species production by an in silico and in vitro study using 3T3-L1 cells. The structures of F1 compound has been obtained from own in-house Panax ginseng saponin data base. In silico molecular docking and drug likeness properties including absorption, distribution, metabolism and excretion, and toxicity and prediction of biological activity were performed in order to assess and investigate the antiobesity activity of F1. Molecular docking study showed that F1 exhibited strong hydrogen binding affinity with Janus activated protein kinase-2 greater than −9.2 Kcal/mol compared to co-crystalized ligand 3kc and nicotinamide (control drug) −8.2 kcal/mol and −4.6 Kcal/mol respectively. In addition, our in vitro results indicated that F1 also showed significant inhibitory effect on the triglyceride content and reactive oxygen species production in adipocyte differentiation. Moreover, F1 significantly reduced the mRNA expression of adipogenesis markers such as peroxisome proliferator-activated receptor gamma, adipocyte fatty acid-binding protein, and Janus activated prot, which are responsible for lipid accumulation. Our findings demonstrated that ginsenoside F1 inhibits lipid accumulation and reactive oxygen species generation by downregulating the expression adipocyte differentiation markers in mature 3T3-L1 cells.