Dexamethasone reduces the formation of thoracic aortic aneurysm and dissection in a murine model

Thoracic aortic aneurysm and dissection (TAAD) is a life-threatening vascular disease with no effective pharmaceutical therapies currently available. Inflammation plays a key role in the progression of aneurysms. Dexamethasone (DEX), a synthetic glucocorticoid, has showed alleviating effects on cells in vitro from TAAD patients. Here we performed a study aiming at investigating the protective role of DEX in a β-aminopropionitrile monofumarate (BAPN)-induced TAAD mouse model. DEX (dose: 0.04 mg/kg/day) treatment significantly reduced the aortic diameter and inhibited TAAD formation. DEX reduced infiltration of macrophages and neutrophils, apoptosis of vascular smooth muscle cells (VSMCs), expression of metalloproteinase 2/9, and extracellular matrix degradation in BAPN-treated TAAD mice. Furthermore, DEX therapy downregulated the expression of p-p65 in macrophages and VSMCs, which suggested that DEX might ameliorate BAPN-induced TAAD by suppressing NF-κB signaling. Therefore, DEX therapy attenuates the progression of BAPN-induced TAAD murine model and could be used as an effective adjuvant therapy for treating TAAD. •Dexamethasone attenuated thoracic aortic aneurysm and dissection in a mouse model.•Dexamethasone reduced infiltration of inflammatory cell and apoptosis of vascular smooth muscle cell and fibroblast.•Dexamethasone partly alleviated degradation of collagen and phenotype switch.•DEX might ameliorate thoracic aortic aneurysm and dissection by suppressing NF-κB signaling pathway.