Objective To establish the vulnerable atherosclerotic plaque model with rabbits and treat them with intravenous infusion of bone marrow mesenchymal stem cells (MSCs) , so as to verify the impact of MSCs on the stability of vulnerable plaque (VP). Methods Totally 24 healthy male New Zealand white rabbits were randomly divided into three groups. Carotid vulnerable atherosclerotic plaque models were made with rabbits in VP group (n=8) and VP+MSCs group (n=8); VP+MSCs group was given intravenous infusion of 1×10⁷ MSCs immediately after modeling and VP group was infused with phosphate buffer. Stable atherosclerosis plaque model was made with rabbit in SP group (n=8). Animals in all groups were sacrificed at the end of the 12^th week, and the right common carotid arteries were collected and subjected to H-E staining and Masson staining, and the cap/core ratio of atherosclerotic plaque was measured. MMP-2 content was examined by immunohistochemistry. Results H-E staining. In VP group the plaque showed a large lipid core and thin fibrous cap, remnants of foam cells and many inflammatory cells were seen in the plaque shoulder, and some showed rupture plaques and/or thrombosis. In SP group, the structure of plaque was in integrity, with thick fibrous cap and fewer inflammatory cells, and with no plaque rupture. The plaque structure of VP+MSCs group was between those of the other two groups. The order of cap/core ratio was SP group >VP+MSCs group >VP group, with that of VP group being significantly different from those of the other two groups (P<0.01). Masson staining. The contents of muscle fiber and elastic fiber were the highest in SP group, followed by VP+MSCs group, and then by VP group. The level of MMP-2 in VP group was significantly higher than those in the other two groups(P<0. 01), and that in VP+MSCs group was significantly higher than that in SP group (P<0.01). Conclusion Intravenous infusion of MSCs can improve the stability of plaques in VP rabbit model, which may be associated with the reduction of inflammatory cells and MMP-2 level, and the subsequent reduction of collagen fiber degradation.