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腹动脉瘤破裂的新型帕帕因-弹性诱导的小鼠模型

Mohamed Zayed¹, Santiago Elizondo-Benedetto¹, Batool Arif¹

¹Washington University in St. Louis.

Research square

|August 20, 2025

概括

开发腹腔大动脉瘤 (AAA) 破裂的新动物模型至关重要. 将猪胰腺弹性酶和帕帕因与β-aminopropionitrile或angiotensin II结合起来,有效地在小鼠中创建了可靠的AAA破裂模型.

科学领域:

血管生物学
外科病理学
动物模型

背景情况:

腹腔大动脉瘤 (AAA) 破裂导致显著的死亡率.
现有的动物模型无法可靠地复制内AAA破裂.
像PPE,Pap,BAPN和ANG II这样的化学剂可以在动物中诱导AAA.

研究的目的:

开发慢性腹腔大动脉瘤 (AAA) 和急性AAA破裂的可靠小鼠模型.
研究化学剂在AAA诱导和破裂中的联合作用.
建立更好地模仿人类AAA病理的模型.

主要方法:

雄性C57BL/6小鼠接受了猪胰腺弹性酶 (PPE),帕帕因 (Pap) 或组合 (PPE + Pap) 的周周暴露.
药物与贝塔- 氨基尼特 (BAPN) 和血管素II (ANG II) 配合或不配合使用.
评估了大动脉直径,炎症,弹性酶降解,矩阵金属酶 (MMP) 活性和破裂率.

主要成果:

帕帕因和PPE+Pap治疗增加了主动脉直径,炎症,弹性酶降解和MMP活性.
添加BAPN诱导了大量的慢性AAA (500%的增长) 和内血栓 (ILT) 的形成.
ANG II治疗导致93%的破裂率,炎症增加,MMP激活和ILT形成.

结论:

结合化学剂的新型小鼠模型可靠地诱导慢性AAA和急性破裂.
这些模型展示了人类AAA的关键病理特征,包括ILT的形成.
开发的模型适用于AAA病理生理学研究和治疗发现.

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