黑色素通过抑制S100a9介导的血管炎症来缓解动脉样硬化
Liyuan Chen1, Xue Wang2, Chang Liu3
1Department of Cardiology, Southwest Hospital, Third Military Medical University, Chongqing, 400038, China.
European journal of pharmacology
|August 25, 2023
概括
黑色素治疗通过抑制S100a9/NF-κB通路来减少动脉样硬化 (AS). 这一发现揭示了黑激素在治疗AS和血管炎症方面的新治疗机制.
科学领域:
- 心血管研究研究心血管研究
- 内分泌学 在内分泌学.
- 炎症生物学 炎症生物学
背景情况:
- 动脉样硬化 (AS) 是全球死亡的主要原因.
- 黑激素是一种具有抗炎性能的激素,显示出AS治疗的潜力,但其机制尚未完全理解.
- 在AS中研究黑激素的治疗机制对于临床应用至关重要.
研究的目的:
- 阐明黑激素发挥其抗动脉样硬化作用的机制.
- 确定参与黑激素对AS的作用的关键分子介质.
- 探索黑激素作为一种负担得起的AS治疗干预措施的潜力.
主要方法:
- 在使用高脂肪饮食 (HFD) 的apolipoprotein E-deficient (ApoE-/-) 小鼠中诱导了动脉样硬化.
- 黑色素被用腹膜内给药了12周.
- 技术包括免疫组织化学,免疫光,数据独立获取 (DIA) 基础上的蛋白质组学,机智路径分析 (IPA),西部涂抹和腺相关病毒 (AAV) 载体研究.
主要成果:
- 在HFD养的ApoE-/-小鼠中,黑素治疗显著减少了动脉样硬化病变,巨细胞透和促炎性细胞因子的产生.
- 蛋白质组分析发现S100a9是黑激素保护作用的关键调解者.
- 黑色素抑制了HFD诱导的S100a9表达,这反过来又抑制了NF-κB信号通路和血管炎症.
结论:
- 黑色素通过抑制S100a9 / NF-κB信号通路,显示出显著的抗动原效应.
- 这项研究揭示了黑激素抗动脉样硬化作用的新机制.
- 黑色素作为一种临床上可用的,负担得起的治疗剂,有望调节AS.
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