Dehydroepiandrosterone (脱氢表雄酮，DHEA，AbMole，M9061)是一种雄激素受体(AR)和神经甾体受体的激动剂。Dehydroepiandrosterone（Prasterone， CAS No.：53-43-0）参与调节细胞的增殖、凋亡、代谢稳态及免疫功能。例如Dehydroepiandrosterone 可抑制SK-Hep-1肝癌细胞系的增殖并诱导细胞线粒体功能紊乱，表现为能量代谢障碍和增殖率显著下降[1]。类似地，Dehydroepiandrosterone（Dehydroisoandrosterone）在结直肠癌（CRC）细胞中，通过诱导内质网应激（ER stress）激活PERK/eIF2/ATF4/CHOP信号通路，进而触发自噬与凋亡[2]。Dehydroepiandrosterone（脱氢表雄酮，DHEA，AbMole，M9061）在动物模型中可以调节动物的代谢和生殖系统，并且还是小鼠、大鼠等啮齿动物多囊卵巢综合征（PCOS）模型构建的重要工具[3]。此外，Dehydroepiandrosterone还可以改善小鼠的胰岛素抵抗[4]。

范例详解

Biol Sex Differ. 2025 Dec 23;16(1):107.

兰州大学的科研人员在上述论文中使用了AbMole的Dehydroepiandrosterone (脱氢表雄酮，Prasterone，DHEA，AbMole，M9061)和Sitagliptin（AbMole，M5965）。其中DHEA被用于构建大鼠多囊卵巢综合征（PCOS）模型。实验人员在该模型上探究了PCOS大鼠中DPP4蛋白调节铁死亡的机制，及其对子宫内膜容受性影响的研究。研究发现PCOS大鼠子宫内膜存在Fe²⁺积累、抗氧化功能障碍、线粒体损伤等铁死亡特征。此外，科研人员通过Sitagliptin抑制DPP4可改善大鼠妊娠前的蜕膜化反应和容受性标志物，下调DPP4可抑制T-HESCs的激素受体表达和铁死亡标志物。

Medium dose of sitagliptin ameliorated PCOS-like phenotype and ferroptosis in the endometrium of PCOS rats[5]

参考文献及鸣谢

[1] Cheng, M. L.; Chi, L. M.; Wu, P. R.; et al. Dehydroepiandrosterone-induced changes in mitochondrial proteins contribute to phenotypic alterations in hepatoma cells. Biochemical pharmacology 2016, 117, 20-34.

[2] Nguyen, T. H.; Ko, H. J.; Tsai, P. Y.; et al. Dehydroepiandrosterone suppresses human colorectal cancer progression through ER stress-mediated autophagy and apoptosis in a p53-independent manner. Frontiers in pharmacology 2024, 15, 1464647.

[3] Zhang, Y.; Xie, X.; Han, L. Connection between granulosa cell pyroptosis and oocyte endoplasmic reticulum stress in a mouse model of polycystic ovary syndrome. Journal of ovarian research 2025, 18 (1), 288.

[4] Aoki, K.; Terauchi, Y. Effect of Dehydroepiandrosterone (DHEA) on Diabetes Mellitus and Obesity. Vitamins and hormones 2018, 108, 355-365.

[5] Zhang, J.; Wang, R.; Tian, X.; et al. The mechanism study of targeting DPP4 in regulating ferroptosis and its influence on endometrial receptivity in PCOS. Biology of sex differences 2025, 16 (1), 107.