Abstract
In the present study, we evaluated the effects of dietary histone deacetylase inhibitor sulforaphane on cell proliferation and adipogenesis in pre‐adipocytes. Mouse 3T3‐L1 pre‐adipocytes were pre‐treated with six different phytochemicals and differentiated into adipocytes. The results showed that sulforaphane significantly decreased cell viabilities of 3T3‐L1 cells compared to other phytochemicals. Furthermore, Oil Red O staining indicated that adipogenesis was inhibited by sulforaphane in a dose‐dependent manner. To understand the molecular mechanisms involved in adipogenesis inhibition by sulforaphane, we carried out oligo DNA microarray analysis. Among down‐regulated genes, we selected five genes involved in lipid metabolism and down‐regulation of those genes was confirmed by RT‐PCR and quantitative real‐time PCR. In addition, 3T3‐L1 cells were incubated with trichostatin A, sulforaphane or 5‐aza‐deoxycytidine during adipocyte differentiation and then lipid formation was evaluated with expression level of mLeptin. Interestingly, the histone deacetylase inhibitor trichostatin A and sulforaphane suppressed mLeptin expression, whereas the DNA demethylating agent 5‐aza‐deoxycytidine increased mLeptin expression. These results indicate sulforaphane exerts anti‐obesity effects via mechanisms involving epigenic down‐regulation of adipogeneic genes.
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