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在人类微血管系统中,p,p'-Dichlorodiphenyldichloroethylene (p,p'-DDE) 的抗血管效应

Bulbul Ahmed¹, Melissa G Farb¹, Kimberly Chen¹

¹Evans Department of Medicine and Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, MA, USA.

Toxicology in vitro : an international journal published in association with BIBRA

|November 13, 2025

概括

农药代谢物p,p'-DDE通过降低FGF2的调节来损害人类的微血管功能. 这一发现揭示了一个新的机制,将环境污染物与心血管疾病风险联系起来.

科学领域:

环境健康环境健康
心血管生物学心血管生物学
内分泌学在内分泌学.

背景情况:

p,p'-Dichlorodiphenyldichloroethylene (p,p'-DDE) 是一种持久性农药代谢物,在人体内生物积累.
p,p'-DDE与内分泌干扰,癌症和潜在的心血管疾病有关,但潜在的机制尚不清楚.

研究的目的:

为了研究p,p'-DDE对人类血管性微血管功能的影响.
阐明p,p'-DDE影响内皮细胞和微血管健康的分子机制.

主要方法:

从减肥手术患者的血中分析p,p'-DDE水平.
活体评估p,p'-DDE对脂肪组织微血管血管生成能力的影响.
使用人类大动脉内皮细胞 (HAEC) 进行体外研究,以检查基因表达变化.

主要成果:

在所有受试者中检测到p,p'-DDE,超过其母化合物的水平.
活体暴露于p,p'-DDE显著损害了脂肪组织的微血管功能.
在HAEC中,p,p'-DDE剂量依赖下调的纤维细胞生长因子2 (FGF2) 基因表达.
外源性FGF2补充完全逆转了p,p' - DDE诱导的血管功能障碍.

结论:

p,p'-DDE干扰人类的微血管血管新生过程,主要是通过降低FGF2.
这项研究提供了一种新的机制,将环境污染物暴露 (p,p'-DDE) 与心血管健康不良结果联系起来.

关键词:

肥胖的是一种脂肪.血管新生的产生.在P,p-DDE中.

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