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Sulforaphane attenuates bisphenol A-induced 3T3-L1 adipocyte differentiation through cell cycle arrest
•We investigate the effect of sulforaphane on BPA-induced 3T3-L1 adipogenesis.•Sulforaphane inhibit BPA-induced 3T3-L1 adipocyte differentiation.•Sulforaphane suppress BPA-induced cell cycle progression during an early stage of adipogenesis.•Sulforaphane stimulate MAPK pathway.•Sulforaphane regulate...
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Published in: | Journal of functional foods 2018-05, Vol.44, p.17-23 |
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Main Authors: | , , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | •We investigate the effect of sulforaphane on BPA-induced 3T3-L1 adipogenesis.•Sulforaphane inhibit BPA-induced 3T3-L1 adipocyte differentiation.•Sulforaphane suppress BPA-induced cell cycle progression during an early stage of adipogenesis.•Sulforaphane stimulate MAPK pathway.•Sulforaphane regulate AMPK pathway.
Bisphenol A (BPA) may be a critical risk factor for metabolic disorders including obesity and diabetes. Sulforaphane is known to inhibit adipocyte differentiation and induce adipocyte lipolysis. This study sought to investigate the possible effects of sulforaphane on BPA-induced adipocyte differentiation in 3T3-L1 cells. During the preadipocytes differentiation process, sulforaphane suppressed the expression of early adipogenic factors, PPARγ and C/EBPα, induced by BPA in 3T3-L1 cells. Based on cell cycle analysis, sulforaphane mediated the inhibition of mitotic clonal expansion via cell cycle arrest at the G0/G1 phase. The compound inhibited cell cycle progression by suppressing cell cycle regulators such as cyclin D1 and pRb and by increasing p21 and p27, cell cycle inhibitors. Moreover, sulforaphane activated phosphorylation of AMPK and ACC and decreased that of ERK1/2 and Akt. Sulforaphane exerts inhibitory effects on BPA-induced adipocyte differentiation in 3T3-L1 cells. Sulforaphane could be adipogenic properties for improving environmental pollutants. |
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ISSN: | 1756-4646 2214-9414 |
DOI: | 10.1016/j.jff.2018.02.021 |