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Inflammation plays a pivotal role in the development of abdominal aortic aneurysms (AAAs).The purpose of the study was to elucidate molecular mechanisms that might orchestrate leukocyte recruitment into the outer wall by determining whether CC chemokines contribute to development of aneurysm degeneration in an nicotine-induced mouse model of AAA and the underlying mechanism.Our results showed that SP600125 (JNK inhibitor) attenuates nicotine-induced aortic aneurysm formation, simultaneously, MCP-1 and RANTES was observed up-regulation significantly in aortic aneurysm lesions compared with normal mouse aorta, and in vitro, nicotine induced the expression of MCP-1and RANTES in both RAW264.7 cells and MOVAS cells in a dose-dependent manner, with an upregulating expression by 0.5ng/ml nicotine but a downregulating expression by 500ng/ml nicotine.Furthermore, the upregulation of expression activation of MCP-1 and RANTES was significantly abrogated by SP600125 or PNU-282987, and transwell migration assay was similar assessed.In conclusion, SP6000125 attenuates nicotine-induced aortic aneurysm formation, nicotine-induced MOVAS cells and RAW264.7 cells express MCP-1 and RANTES in a dose-dependent manner.The expression of chemokines in MOVAS cells induced by nicotine have an effect on RAW264.7 migration, which is likely contribute to the development of aortic aneurysm.