负气离子通过抑制AP1介导的FN1和SPP1来减轻尼古丁诱导的血管内皮功能障碍
Sha Xiao1,2,3, Tianjing Wei1,2, Mingyang Xiao1,2
1Key Laboratory of Environmental Stress and Chronic Disease Control and Prevention, Ministry of Education, China Medical University, Shenyang 110122, China.
Antioxidants (Basel, Switzerland)
|July 29, 2025
概括
负气离子 (NAI) 通过抑制AP1通路来保护高血压中尼古丁诱导的内皮功能障碍. 这项研究为减少与吸烟相关的心血管风险提供了新的见解.
科学领域:
- 心血管科学 心血管科学
- 环境健康 环境健康
- 分子生物学分子生物学
背景情况:
- 尼古丁诱导的氧化应激会损害血管内皮功能,这是高血压的关键因素.
- 负气离子 (NAI) 显示出血压调节和抗氧化作用的潜力,但其机制尚未完全理解.
研究的目的:
- 在自发高血压大鼠 (SHRs) 中研究NAI对尼古丁诱导的氧化损伤和内皮损伤的保护作用.
- 阐明涉及α7nAChR/MAPK/AP1通路的分子机制,并确定由NAI调节的关键基因.
主要方法:
- 西部涂抹用于分析α7nAChR/MAPK/AP1通路.
- 转录组测序以识别差异表达的基因.
- 在人类大动脉内皮细胞 (HAEC) 中测量反应性氧物种 (ROS),内甲素-1 (ET-1) 和细胞内 ([Ca2+]i).
- 染色体免疫沉定量PCR (ChIP-qPCR) 测定AP1与目标基因之间的关系.
主要成果:
- 尼古丁通过α7nAChR/MAPK/AP1激活在SHR中引起血压升高,氧化应激和内皮损伤.
- 美国国家药物抑制剂逆转了尼古丁诱导的变化,包括氧化 (NO) /内皮氧化合成酶 (eNOS) 的降低和ET-1/内皮素A受体 (ETab) 表达的增加.
- 在HAEC中,NAI通过抑制AP1介导的纤维素1 (FN1) 和分泌的蛋白1 (SPP1) 的激活来减轻尼古丁诱导的增殖障碍,氧化应激和[Ca2+]i水平.
结论:
- 在高血压中,NAI可以保护尼古丁诱导的内皮功能障碍.
- 保护机制包括抑制AP1转录因子,该因子调节FN1和SPP1的表达.
- 这些发现为减轻吸烟相关心血管风险提供了新的治疗见解.
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