Objective To establish and evaluate a blunt common carotid artery trauma model created by common carotid artery clipping, which can simulate exogenous physical injury. Methods Sixty-four healthy male C57BL/6J mice were randomly divided into sham group, and 1, 3 and 7 d after clipping groups, with 16 mice in each group. The mice in the sham group were given cervical incision suture, and those in the modeling group were given left common carotid artery clipping occlusion for 30 min. Common carotid arteries were then harvested, the vascular structure was observed by hematoxylin-eosin (H-E) staining, and the expression of vascular function related proteins was detected by immunohistochemical staining (n=10) and Western blotting (n=6). Results H-E staining showed that the vascular endothelial cells were injured to different extents, and the integrity of vascular matrix was decreased after carotid artery clipping. Immunohistochemical staining showed that the expression levels of vascular cell adhesion molecule 1 (VCAM-1), endothelial nitric oxide synthase (eNOS) and endothelin-1 were up-regulated after common carotid artery clipping, and the expression of inflammatory cell marker myeloperoxidase (MPO) was also elevated in vascular walls and perivascular tissues.The results of Western blotting showed that the expression levels of vascular function related markers (VCAM-1, eNOS and endothelin-1), inflammation-related proteins (cyclooxygenase 2 [COX-2], matrix metalloproteinase[MMP]-2 and MMP-9), and apoptosis-related proteins (B-cell lymphoma-related X protein[Bax] and cleaved caspase 1) were increased to different extents after common carotid artery clipping. Among them, the expression of VCAM-1 and eNOS peaked 3 d after clipping, and the expression of endothelin-1 showed an upward trend from 1 d to 7 d after clipping. Conclusion A blunt common carotid artery trauma mouse model created by common carotid artery clipping has been successfully established. Common carotid artery clipping can induce vascular tissue injury, inflammation and cellular apoptosis, and it may be an important factor of traumatic vascular stenosis and aneurysm.