Abstract: Objective To evaluate whether colchicine mitigates acute aortic dissection (AAD) in mice and to define its mechanistic basis. Methods Sixty 12-week-old male mice were randomized into control (n=20),model (n=20),and colchicine (Col,n=20) groups. AAD incidence,aortic diameter,and medial architecture were assessed by HE and Verhoeff-Van Gieson staining. Macrophage infiltration (CD68⁺ cells) was quantified by flow cytometry. Systemic and local inflammatory markers (IL-6, TNF-α) were measured by ELISA, qPCR, Western blot. Smooth muscle cell (SMC) phenotypic switching and apoptosis were evaluated by α-SMA immunohistochemistry and TUNEL staining,respectively. Apoptosis-related proteins (cleaved caspase-3,total caspase-3,Bax,Bcl-2) and NF-κB pathway components (phosphorylated NF-κB,total NF-κB,IκBα) were analyzed by Western blot. Results Colchicine reduced AAD incidence from 75% to 30% (P＜0.05),limited aortic expansion,and preserved medial thickness with intact elastic lamellae. Macrophage accumulation in the aortic wall was markedly suppressed in the Col group(P＜0.05). Both serum and tissue levels of IL-6 and TNF-α were downregulated by colchicine (P＜0.05). The model group displayed increased SMC apoptosis,loss of α-SMA positivity,an elevated cleaved/total caspase-3 ratio,Bax upregulation,and Bcl-2 downregulation—changes that were attenuated by colchicine (P＜0.05). Mechanistically,the Model group exhibited IκBα degradation and enhanced NF-κB phosphorylation,whereas colchicine stabilized IκBα and suppressed NF-κB activation (P＜0.05). Conclusions Colchicine confers protection against AAD in this murine model by interrupting NF-κB-mediated inflammatory reaction and SMC apoptosis.

Key words: acute aortic dissection, colchicine, inflammatory reaction, apoptosis, nuclear factor-κB