Dioxinodehydroeckol suppresses adipocyte differentiation of 3T3-L1 preadipocytes by MAPK pathway

Dioxinodehydroeckol was isolated from E. Cava and its inhibitory effect on lipid accumulation in cultured 3T3-L1 adipocytes were investigated by measuring TG contents and Oil-Red O staining and changes in genes and proteins associated with adipogenesis and lipolysis. Treatment withdioxinodehydroeckol significantly reduced lipid accumulation during adipocyte differentiation and induced down-regulation of SREBP1, PPARγ and C/EBPα in a dose-dependent manner. Moreover, dioxinodehydroeckol suppressed regulation of the adipocyte specific gene promoters such as FABP4, FATP1, FAS, LPL, ACS1 and leptin. As the lipolytic response, dioxinodehydroeckol down-regulated expression levels of perilipin and HSL genes and up-regulated the expression levels of TNFa mRNA compared to fully differentiated adipose tissue. Specific mechanism of dioxinodehydroeckol was examined through transcriptional downregulations of extracellular signal-regulated kinase (ERK). Therefore, these results suggest that dioxinodehydroeckol induced antiadipogenic effect on adipocytes via ERK-dependent signaling pathway.