Exploring the inhibitory effects of Brassica juncea extract and sinigrin on lipid accumulation in BPA-Induced 3T3-L1 cells via the glucocorticoid receptor and peroxisome proliferator-activated receptor-γ pathways

초록

Obesogens, such as bisphenol A (BPA), are emerging models for obesity research, yet their mechanisms remain less explored. While BPA has been extensively studied for its estrogen receptor interactions, its effects on the glucocorticoid receptor (GR) remain unclear. This study explored the role of the GR in BPA-induced lipid accumulation using the GR antagonist mifepristone (10 mu M) and the PPAR-gamma antagonist GW9662 (15 mu M) in 3T3-L1 preadipocytes. Both antagonists significantly reduced BPA-induced lipid accumulation. Furthermore, co-treatment with Brassica juncea extract (BJE, 800 mu g/mL) or its bioactive component sinigrin (36 mu M) alongside the antagonists preserved the inhibitory effect on lipid accumulation without compromising cell viability. Mechanistic investigations revealed that BJE and sinigrin suppressed phospho-GR and PPAR-gamma protein expression. Overall, the findings indicate that BPA promotes adipocyte differentiation via both GR and PPAR-gamma pathways and that BJE and sinigrin may serve as natural anti-obesogenic agents targeting these mechanisms.

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