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<p>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&#xa0;μM) and the PPAR-γ antagonist GW9662 (15&#xa0;μM) in 3T3-L1 preadipocytes. Both antagonists significantly reduced BPA-induced lipid accumulation. Furthermore, co-treatment with <i>Brassica juncea</i> extract (BJE, 800&#xa0;μg/mL) or its bioactive component sinigrin (36&#xa0;μM) 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-γ protein expression. Overall, the findings indicate that BPA promotes adipocyte differentiation via both GR and PPAR-γ pathways and that BJE and sinigrin may serve as natural anti-obesogenic agents targeting these mechanisms.</p>

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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

  • 期刊论文

  • 发表日期：

    2025年6月13日

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  • Ji-Hyun Im,
  • Geon Oh,
  • Xiaolu Fu,
  • June seok Lim,
  • Min-Hye Kim,
  • Yeon-Seok Seong,
  • Sun-Il Choi,
  • Ok-Hwan Lee

摘要

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 μM) and the PPAR-γ antagonist GW9662 (15 μM) in 3T3-L1 preadipocytes. Both antagonists significantly reduced BPA-induced lipid accumulation. Furthermore, co-treatment with Brassica juncea extract (BJE, 800 μg/mL) or its bioactive component sinigrin (36 μM) 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-γ protein expression. Overall, the findings indicate that BPA promotes adipocyte differentiation via both GR and PPAR-γ pathways and that BJE and sinigrin may serve as natural anti-obesogenic agents targeting these mechanisms.