Chen Shuxiao, Liu Xiaotian, Zhou Xincheng, Lin Weixiao, Liu Minting, Ma Haoran, Zhong Keli, Ma Qiming, Qin Chengjian
Department of Bariatric Surgery, The First Affiliated Hospital of Jinan University, Guangzhou, China.
Clinical Medicine, International College of Jinan University, Guangzhou, China.
Front Immunol. 2025 Jan 31;16:1486072. doi: 10.3389/fimmu.2025.1486072. eCollection 2025.
Abdominal aortic aneurysm (AAA) is a degenerative disease with high mortality. Chronic inflammation plays a vital role in the formation of AAA. Atractylenolide-I (ATL-I) is a major bioactive component of Rhizoma Atractylodis Macrocephalae that exerts anti-inflammatory effects in various diseases. The purpose of this study is to investigate the role of ATL-I in the progression of AAA.
AAA was constructed in C57BL/6 mice by porcine pancreatic elastase (PPE)-incubation, and the diameter of the aorta was measured by ultrasound. ATL-I was administered by gavage on the second day after modeling to explore its significance in AAA. The pathological and molecular alteration was investigated by immunostaining, ELISA, qRT-PCR and Western blotting.
ATL-I inhibited the dilatation of the abdominal aorta and decreased the incidence of AAA. ATL-I alleviated the infiltration of macrophages in the adventitia and reduced the levels of proinflammatory factor IL-1β and IL-6 in the aorta and circulatory system, while increasing the expression of anti-inflammatory factor IL-10. Moreover, ATL-I restrained loss of smooth muscle cells and elastic fiber degradation by suppressing MMP-2 and MMP-9 expression. Mechanistically, phospho-AMPK expression was elevated in AAA groups, and ATL-I administration suppressed its expression to improve the pathological damage of aorta.
ATL-I meliorated vascular inflammation by targeting AMPK signaling, ultimately inhibiting AAA formation, which provided an alternative agent for AAA treatment.
腹主动脉瘤（AAA）是一种死亡率很高的退行性疾病。慢性炎症在AAA的形成中起着至关重要的作用。白术内酯-I（ATL-I）是白术的主要生物活性成分，在多种疾病中发挥抗炎作用。本研究旨在探讨ATL-I在AAA进展中的作用。
通过猪胰弹性蛋白酶（PPE）孵育在C57BL/6小鼠中构建AAA，并通过超声测量主动脉直径。在建模后第二天通过灌胃给予ATL-I，以探讨其在AAA中的意义。通过免疫染色、酶联免疫吸附测定、定量逆转录聚合酶链反应和蛋白质印迹法研究病理和分子改变。
ATL-I抑制腹主动脉扩张并降低AAA的发生率。ATL-I减轻了外膜中巨噬细胞的浸润，降低了主动脉和循环系统中促炎因子IL-1β和IL-6的水平，同时增加了抗炎因子IL-10的表达。此外，ATL-I通过抑制MMP-2和MMP-9的表达来抑制平滑肌细胞的丢失和弹性纤维的降解。机制上，AAA组中磷酸化AMPK表达升高，给予ATL-I可抑制其表达，改善主动脉的病理损伤。
ATL-I通过靶向AMPK信号改善血管炎症，最终抑制AAA形成，为AAA治疗提供了一种替代药物。
