Abstract: Objective　To investigate the effect of electrical stimulation of vagus nerve on migration and differentiation of c-kit+ vascular wall cells in rats under carotid artery injury. Methods　A total of 24 SD rats were randomly divided into three groups: the sham-operation group, the operation group and the vagus nerve stimulation group, with 8 rats in each group. After the common carotid artery balloon injury model was carried out, the left vagus nerve was electrically stimulated in the vagus nerve stimulation group. HE staining and immunohistochemical staining were used to observe the thickness of vascular intima and the distribution of c-kit+ vascular wall cells. The serum levels of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) were measured by enzyme-linked immunosorbent assay (ELISA). After isolating c-kit+ cells from the vessel wall, the c-kit+ cells were divided into three groups：the control group (no acetylcholine), the 10-5 mol/L acetylcholine group and the 10-5 mol/L acetylcholine group with the + alpha 7 nicotinic acetylcholine receptor (α7nAChR) agonist group. Transwell assay was applied to detect the effect of acetylcholine on c-kit+ migration, and the expression of smooth muscle 22 alpha (SM22α) was detected by Western blot assay. Results　(1) Compared with operation group, the thickness of vascular neointima was reduced, and the number of c-kit+ cells in vascular neointima was decreased in the vagus nerve stimulation group (P＜0.05), and the serum levels of TNF-α and IL-6 were also reduced (P＜0.01). (2) Acetylcholine inhibited the c-kit+ migration and increased the expression of SM22α, which could be reversed by α7nAChR agonist. Conclusion　Acetylcholine can mitigate the neointimal formation through inhibiting the migration of c-kit+ and accelerating the differentiation of c-kit+ to vascular smooth muscle cells, the mechanism of which may be related to acetylcholine combined with α7nAChR that activating anti-inflammatory system.

Key words: vagus nerve, electric stimulation, acetylcholine, proto-oncogene proteins c-kit, alpha7 nicotinic acetylcholine receptor, neointimal formation, c-kit+ cells