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蒙特卢卡斯特通过激活AMPK/mTOR信号通路,在小鼠中抑制腹腔大动脉动脉瘤的形成

Jian Huang¹, Jiawei Zhuang¹, Jiamao Wang¹

¹The First Affiliated Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, 361000, China.

Langenbeck's archives of surgery

|November 27, 2024

概括

蒙特卢卡斯特通过调节AMPK/mTOR通路,有效地抑制小鼠腹腔大动脉动脉瘤 (AAA) 的形成. 这种治疗减少了细胞亡,炎症和矩阵金属蛋白酶水平,为AAA提供了潜在的治疗策略.

科学领域:

心血管研究研究心血管研究
药理学药理学是指药理学的学科.
分子生物学分子生物学

背景情况:

腹腔大动脉瘤 (AAA) 是一种危及生命的疾病,其特征是腹腔大动脉扩张.
AAA形成的基本机制包括炎症,细胞亡和细胞外矩阵降解.
针对特定的信号通路为AAA治疗提供了潜在的治疗途径.

研究的目的:

在小鼠模型中阐明蒙特卢卡斯特对AAA形成的抑制机制.
调查AMP激活蛋白激酶 (AMPK) /哺乳动物目标拉巴胺素 (mTOR) 信号通路在蒙特卢卡斯特对AAA的影响中的作用.
在AAA中评估蒙特卢卡斯特对亡,炎症和矩阵金属蛋白酶活性的影响.

主要方法:

在小鼠中使用 ангиотензинII输液诱导AAA.
小鼠接受了蒙特卢卡斯特治疗,单独或与化合物C (AMPK抑制剂) 结合治疗.
评估了血管重塑,细胞亡 (TUNEL染色),以及关键标记物 (Bax,Bcl-2,MMPs,炎症细胞因子,p-AMPK/AMPK,p-mTOR/mTOR) 的蛋白质/基因表达 (西布洛特,qRT-PCR).

主要成果:

与Ang II诱导的模型相比,蒙特卢卡斯特治疗显著降低了AAA直径,发生率和大动脉壁厚度.
蒙特卢卡斯特降低了细胞亡,炎症性细胞因子表达 (IL-6,TNF-α,IFN-γ) 和矩阵金属蛋白酶 (MMP-2,MMP-9).
蒙特卢卡斯特的使用上调了p-AMPK/AMPK和下调了p-mTOR/mTOR,表明AMPK/mTOR通路的激活;这些效应被C化合物逆转.

结论:

蒙特卢卡斯特在抑制小鼠AAA形成方面表现出显著的疗效.
蒙特卢卡斯特的保护作用通过AMPK/mTOR信号通路进行介导.
蒙特卢卡斯特的机制涉及细胞亡,炎症反应和矩阵金属蛋白酶活性的下调.

关键词:

在AMPK/mTOR中使用.腹腔大动脉动脉瘤腹腔大动脉动脉瘤细胞灭亡 (apoptosis) 是一种死亡的过程.炎症炎症是一种炎症.矩阵金属蛋白酶是一种金属蛋白酶.蒙特利卢卡斯特是一个蒙特利卢卡斯特.

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