动物造模 z-bio 2022-07-20 297

　　Objective: To study the role of calcineurin (CaN) and its downstream activated T cell nuclear factor (NFATc3) in restenosis after balloon dilatation, and to provide a new theoretical basis for the prevention and treatment of vascular restenosis.

　　Methods: Male SD rats were randomly divided into sham operation group (n=12), balloon group (n=12), and cyclosporine (CsA) group (n=12). Rats in the balloon group were treated with balloon dilation to injure the abdominal aorta; the rats in the CsA group were fed with CsA 12.5 mg/(kg.d)-1 every day from 3 days before the operation to the end of the experiment. 30 days after balloon injury, the samples were taken, the vascular tissue was stained with hematoxylin-eosin (HE) and immunohistochemistry to detect the level of CaN in the vascular wall, and the pathological changes were observed by light microscope; Rea1 time PCR technology was used to detect the CaN in the vascular wall tissue. , NFATc3 mRNA expression; Elisa method to measure serum MCP-1 level.

　　RESULTS: Neointima appeared in the vessel wall after balloon injury, and the thickness was uneven. Compared with the balloon injury group, the intimal hyperplasia and intima/media thickness were significantly reduced in the CsA group (P<0.05). Compared with the sham operation group, the expression of CaN protein and mRNA in the vascular wall tissue of the balloon injury group was significantly increased, the mRNA expression of NFATc3 was significantly increased, and the level of plasma inflammatory factor MCP-1 was also increased (P<0.05). The above indexes in the CsA group were significantly lower than those in the balloon injury group (P<0.05).

　　Conclusion: The CaN-NFATc3 pathway is involved in the occurrence of restenosis after balloon injury in rats; CsA can reduce the formation of restenosis by inhibiting this pathway.