Objective To investigate the expression and significance of the JNK/ c-Jun pathway in the angiotensin II-induced abdominal aortic aneurysm mouse model. Methods C57BL/ 6 Apoe^{- / -} male mice were randomly divided into three groups: sham model, and inhibitor groups. Mice in the sham group were implanted with a preloaded saline micro- release pump in the subscapular scapula, whereas mice in model and inhibitor groups were implanted with an Ang II trace release pump (1000 ng / min·kg). The modeling cycle was 28 days. The inhibitor group was pretreated by intraperitoneal injection of 1 mL/ day JNK inhibitor SP600125 ( 2 mg / kg) for 2 days before surgery. Sham and model groups were administered an equal volume of normal saline. Hematoxylin-eosin staining was used to observe the inflammatory response index of mice. 2′,7′-Dichlorofluorescein-diacetate (DCFH-DA) staining was used to detect the fluorescence intensity of reactive oxygen species (ROS). Western blotting was used to detect expression of p-JNK and p-c-Jun proteins. Results Compared with the sham group, pathological symptoms of AAA tissue in the model group were obvious. Green fluorescence in AAA tissue was enhanced significantly and ROS content was increased significantly. Expression levels of p-JNK and p-c- Jun in AAA tissues were enhanced significantly (all P <0. 05). Compared with the model group, the pathological symptoms of AAA tissue were relatively improved. Green fluorescence in AAA tissue was weakened significantly and ROS content was decreased significantly. The levels of p-JNK and p-c-Jun in AAA tissues were decreased significantly ( P < 0. 05 ). Conclusions The JNK signaling pathway plays an important role in regulation of angiotensin II-induced abdominal aortic aneurysm in mice. Inhibition of this pathway suppresses oxidative stress and improves AAA symptoms.