Abstract: Objective To investigate the effect of nicotine on expression of extracelllular matrix (ECM) and integrin β1 (β1) in vascular smooth muscle cells (VSMCs) of rats in order to explore the possible mechanism of the smoking-induced atherosclerosis. Methods VSMCs isolated from rats were subjected to 100μmol/L nicotine for 24 hours，and the cells without nicotine treatment were used as control. The expression of collagenⅠ, fibronectin and integrin β1 was detected by reverse transcription-polymerase chain reaction (RT-PCR), and the p38 activity was detected by Western blotting. Results Compared with the control group, the expression of ECM including collagenⅠ, fibronectin, and integrin β1, and the cell membrane receptor significantly increased in nicotine group, and were respectively 1.8 times, 1.7 times, and 1.6 times higher than the control group (EM>P/EM> <0.05). The p38 activity, increased 1.95 folds (EM>P/EM> <0.01). After incubation with SB202190, specific inhibitor of p38, the higher expression of collagen I induced by nicotine was depressed. BR>Conclusion P38 promotes the high secretion of extracellular matrix induced by nicotine in vitro, suggesting that the higher

Key words: Nicotine, Vascular smooth muscle cells, Extracellular matrix, Integrin, Reverse transcription-polymerase chain reaction, Western blotting.