p,p'-DDT通过PI3K/AKT途径和氧化应激诱导人子宫内膜基质细胞凋亡。

IF 1.8 Q3 OBSTETRICS & GYNECOLOGY
So Ra Oh, Seung Bin Park, Yeon Jean Cho
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引用次数: 0

摘要

目的:双-[4-氯苯基]-1,1,1-三氯乙烷(DDT)是使用最广泛的合成杀虫剂之一,它是一种干扰内分泌的化学物质,有可能干扰人类生殖系统。DDT及其代谢物之一p,p'-DDT对人类子宫内膜基质细胞(ESC)和健康结果的影响仍然未知。在这项研究中,我们探讨了 p,p'-DDT 是否会通过氧化应激诱导人类 ESCs 细胞增殖和凋亡失衡:我们通过量化与内在和外在途径相关的标记物的表达来评估 ESCs 的细胞凋亡。此外,我们还测量了活性氧(ROS)、抗氧化酶活性和雌激素受体(ER)的水平。我们还检测了涉及活化 B 细胞的核因子卡巴轻链增强子的信号变化:结果:经 1,000 pg/mL p,p'-DDT 处理后,我们观察到 Bax 表达增加,Bcl-2 表达减少,caspases 3、6 和 8 表达增加。我们还注意到,p,p'-DDT 处理后,ROS 的生成增加,谷胱甘肽过氧化物酶的表达减少。此外,p,p'-DDT 处理导致ER表达发生变化,磷脂酰肌醇3-激酶(PI3K)、磷酸蛋白激酶B(phospho-AKT)和磷酸胞外信号调节激酶(phospho-ERK)的蛋白水平升高。PI3K/AKT和ERK通路的激活可能代表了p,p'-DDT促使人体间充质干细胞凋亡的潜在机制,并可能与子宫内膜病变有关。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
p,p'-DDT induces apoptosis in human endometrial stromal cells via the PI3K/AKT pathway and oxidative stress.

Objective: Bis-[4-chlorophenyl]-1,1,1-trichloroethane (DDT), one of the most widely used synthetic pesticides, is an endocrine-disrupting chemical with the potential to interfere with the human reproductive system. The effects of DDT and one of its metabolites, p,p'-DDT, on human endometrial stromal cells (ESCs) and health outcomes remain unknown. In this study, we investigated whether p,p'-DDT induces an imbalance in cell proliferation and apoptosis in human ESCs via oxidative stress.

Methods: We assessed apoptosis in ESCs by quantifying the expression of markers associated with both intrinsic and extrinsic pathways. Additionally, we measured levels of reactive oxygen species (ROS), antioxidant enzyme activity, and estrogen receptors (ERs). We also examined changes in signaling involving nuclear factor kappa-light-chain-enhancer of activated B cells.

Results: Following treatment with 1,000 pg/mL of p,p'-DDT, we observed an increase in Bax expression, a decrease in Bcl-2 expression, and increases in the expression of caspases 3, 6, and 8. We also noted a rise in the generation of ROS and a reduction in glutathione peroxidase expression after treatment with p,p'-DDT. Additionally, p,p'-DDT treatment led to changes in ER expression and increases in the protein levels of phosphatidylinositol 3-kinase (PI3K), phospho-protein kinase B (phospho-AKT), and phospho-extracellular signal-regulated kinase (phospho-ERK).

Conclusion: p,p'-DDT was found to induce apoptosis in human ESCs through oxidative stress and an ER-mediated pathway. The activation of the PI3K/AKT and ERK pathways could represent potential mechanisms by which p,p'-DDT prompts apoptosis in human ESCs and may be linked to endometrial pathologies.

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