动物造模,腹主动脉球囊扩张术后再狭窄 z-bio 2021-07-16 607

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

　　Method: Male SD rats were randomly divided into sham operation group (n=12), balloon group (n=12) and cyclosporine (CsA) group (n=12). The rats in the balloon group damaged the abdominal aorta due to balloon expansion. From 3 days before the operation to the end of the experiment, the rats in the CsA group were given CsA 12.5 mg/(kg.d) -1 every day. Thirty days after balloon injury, samples were taken, blood vessel tissues were stained with hematoxylin-eosin (HE), vascular wall CaN content was detected by immunohistochemistry, and pathological changes were observed under light microscope. Real-time fluorescent quantitative PCR technology is used to detect the levels of CaN and FATc3 in blood vessel wall tissues. mRNA expression; ELISA is used to determine serum MCP-1 levels.

　　Result: After balloon injury, a new intima appeared on the blood vessel wall with uneven thickness. Compared with the balloon injury group, the intimal hyperplasia and the thickness of the intima/media in the CsA group were significantly reduced (Pu003c0.05). ). 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 plasma inflammatory factor MCP-1 level was also increased. P).u003c0.05). The above indicators in the CsA group were significantly lower than those in the balloon injury group (Pu003c0.05).

　　Conclusion: CaN-NFATc3 pathway is involved in the development of restenosis after balloon injury in rats. CsA inhibits the formation of restenosis by blocking this pathway.