16种优先控制的PAH的环境剂量诱导内皮功能障碍:一种体内和体外研究
Jian Liu1, Jiaying He1, Zengquan Liao1
1Guangzhou Key Laboratory of Subtropical Biodiversity and Biomonitoring, Guangdong Provincial Engineering Technology Research Center for Drug and Food Biological Resources Processing and Comprehensive Utilization, School of Life Sciences, South China Normal University, Guangzhou 510631, China.
对多环芳 (PAH) 的环境暴露可以通过诱导内皮功能障碍引起心血管疾病. 这项研究证明了PAHs.
科学领域:
- 环境健康 环境健康
- 毒理学 毒理学 毒理学
- 心血管研究研究心血管研究
背景情况:
- 多环芳 (PAH) 是与心血管疾病 (CVD) 相关的环境污染物.
- 内皮功能障碍是心血管疾病发展的关键早期阶段.
研究的目的:
- 调查慢性暴露于PAHs环境剂量和内皮功能障碍之间的关系.
- 阐明PAHs引起的心血管损伤背后的分子机制.
主要方法:
- 同时对雄性斯普拉格-道利 (SD) 鼠和人类静脉内皮细胞 (HUVECs) 进行16种优先PAHs的治疗.
- 暴露时间:老鼠90天,HUVECs48小时.
- 分析炎症标志物,氧化应激,SIRT1和eNOS表达,血管活性物质,细胞粘附,血管形态和血压.
主要成果:
- 暴露于PAH增加了血清TNF-α和MDA水平,并降低了HUVEC和老鼠大动脉中的SIRT1表达.
- PAHs改变了内皮氧化合成酶 (eNOS) 酸化,在HUVEC中增加了内皮蛋白-1 (ET-1) 和血管新生素II (Ang II),并提高了内脏水平.
- PAHs诱导了血管光滑肌肉障碍,增加了THP-1细胞对HUVEC的粘附,并显著提高了大鼠的缩血压.
结论:
- 长期暴露于环境PAHs会在老鼠和HUVEC中诱导内皮功能障碍.
- 通过涉及炎症,氧化应激和血管平衡的破坏的机制,PAHs有助于心血管损伤.
- 研究结果提供了关于预防和干预与环境因素相关的心血管疾病的见解.
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