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Background <p>In our previous animal experiments, we found that caffeic acid phenethyl ester (CAPE) inhibited the early formation of elastase-induced abdominal aortic aneurysms (AAA) in rats. However, its efficacy in the angiotensin II (Ang II)-induced AAA model and the underlying mechanism remain unclear. Therefore, the primary aim of this study was to further validate the potential mechanism of CAPE through in vivo and in vitro experiments utilizing Ang II.</p> Methods and results <p>ApoE<sup>−/−</sup> mice were randomly divided into three groups: Sham group, Ang II model group, and Ang II + CAPE group. Mouse aortic smooth muscle cells (MOVAS) were pretreated with CAPE (0.25 and 0.5 µM) for 1&#xa0;h or the NF-κB inhibitor BAY11-7082 (0.5 µM) for 0.5&#xa0;h, followed by stimulation with Ang II (1 µM) for 24&#xa0;h. In vivo, CAPE intervention significantly reduced the maximum diameter of the aorta, counteracted the increase in osteopontin (OPN) levels in AAA tissue, and restored the decrease in α-smooth muscle actin (α-SMA) expression observed in the model group. Moreover, serum levels of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) were markedly decreased in the Ang II+CAPE group compared to the Ang II model group. In vitro, CAPE treatment significantly inhibited proliferation, migration, invasion and ROS production. It also reduced the apoptosis rate from 9.24 ± 0.60% to 6.11 ± 0.85% (0.25µM CAPE) and 6.00 ± 0.32% (0.5µM CAPE), accompanied by a decreased BAX/BCL-2 ratio. Furthermore, CAPE suppressed the expression of matrix metalloproteinases (MMPs), and OPN, suppressed activation of the NF-κB pathway, and restored α-SMA levels.</p> Conclusions <p>CAPE mitigates the progression of AAA in mice and counteract the abnormal cell phenotype and inflammatory responses in Ang II-stimulated MOVAS cells. These protective effects might be achieved by inhibiting the NF-κB pathway.</p>

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Caffeic acid phenethyl ester attenuates phenotypic switching and inflammation in abdominal aortic aneurysm via the NF-κB pathway

  • 期刊论文

  • 发表日期：

    2026年5月11日

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  • Yuanyuan Gu,
  • Chunshui Cao,
  • Jian Liu,
  • Yong Liu,
  • Liang Huang,
  • Zuan Zhan

摘要

Background

In our previous animal experiments, we found that caffeic acid phenethyl ester (CAPE) inhibited the early formation of elastase-induced abdominal aortic aneurysms (AAA) in rats. However, its efficacy in the angiotensin II (Ang II)-induced AAA model and the underlying mechanism remain unclear. Therefore, the primary aim of this study was to further validate the potential mechanism of CAPE through in vivo and in vitro experiments utilizing Ang II.

Methods and results

ApoE−/− mice were randomly divided into three groups: Sham group, Ang II model group, and Ang II + CAPE group. Mouse aortic smooth muscle cells (MOVAS) were pretreated with CAPE (0.25 and 0.5 µM) for 1 h or the NF-κB inhibitor BAY11-7082 (0.5 µM) for 0.5 h, followed by stimulation with Ang II (1 µM) for 24 h. In vivo, CAPE intervention significantly reduced the maximum diameter of the aorta, counteracted the increase in osteopontin (OPN) levels in AAA tissue, and restored the decrease in α-smooth muscle actin (α-SMA) expression observed in the model group. Moreover, serum levels of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) were markedly decreased in the Ang II+CAPE group compared to the Ang II model group. In vitro, CAPE treatment significantly inhibited proliferation, migration, invasion and ROS production. It also reduced the apoptosis rate from 9.24 ± 0.60% to 6.11 ± 0.85% (0.25µM CAPE) and 6.00 ± 0.32% (0.5µM CAPE), accompanied by a decreased BAX/BCL-2 ratio. Furthermore, CAPE suppressed the expression of matrix metalloproteinases (MMPs), and OPN, suppressed activation of the NF-κB pathway, and restored α-SMA levels.

Conclusions

CAPE mitigates the progression of AAA in mice and counteract the abnormal cell phenotype and inflammatory responses in Ang II-stimulated MOVAS cells. These protective effects might be achieved by inhibiting the NF-κB pathway.