This study was performed to evaluate the effect of monobutyl phthalate (MBP) on GPR30-activated pathways in Sertoli cells. Additionally, we tested if GIM-1 (Panax ginseng metabolite) modulates MBP action. Human Sertoli cells (HSeC lineage) were exposed to MBP and/or GIM-1 for 30 min, 1, 12, and 48 h. Four experimental treatments were performed: control (DEMEM/F12 medium), MBP, GIM-1, and MBP + GIM-1. The results indicate that MBP activates GPR30, PKA, Src, EGFR, and the ERK1/2 proteins, while GIM-1 inhibits PKA, Src, ERK1/2, and the AKT pathway. MBP also enhances Cofilin expression, decreasing F-actin intensity on the cell surface in a short time. The combined exposure demonstrated a functional antagonism between compounds. Collectively, these data show that MBP activates GPR30 in Sertoli cells, and GIM-1 modulates this response, playing a protective role in Sertoli cells exposed to MBP.

本研究旨在评估邻苯二甲酸单丁酯 (MBP) 对支持细胞中 GPR30 激活通路的影响。此外，我们测试了 GIM-1（人参代谢物）是否调节 MBP 作用。将人类支持细胞（HSeC 谱系）暴露于 MBP 和/或 GIM-1 30 分钟、1、12 和 48 小时。进行了四种实验处理：对照（​​DEMEM/F12 培养基）、MBP、GIM-1 和 MBP + GIM-1。结果表明，MBP 激活 GPR30、PKA、Src、EGFR 和 ERK1/2 蛋白，而 GIM-1 抑制 PKA、Src、ERK1/2 和 AKT 通路。MBP 还增强 Cofilin 的表达，在短时间内降低细胞表面的 F-肌动蛋白强度。联合暴露证明了化合物之间的功能拮抗作用。总的来说，这些数据表明 MBP 激活支持细胞中的 GPR30，而 GIM-1 调节这种反应，