The Role And Mechanism Of NGAL Signaling Pathways In The Early Stage Of Porcine Vein Graft Restenosis

Objective: Testing the expression of NGAL signaling pathways in the early stage of porcine vein graft restenosis,to explore the possible role and mechanism in the early narrow vein bridge after coronary artery bypass surgery.Materials and Methods: Collecting samples of the narrow vein bridge vascular in the preoperative and postoperative 7days,14 days,30days of pigs,total of three time points to do the research.Using HE staining and Masson staining,immunohistochemical method,observe the neointimal hyperplasia,the migration of smooth muscle cells and and vascular remodeling of the vein bypass graft,and test the expression changes of NGAL,MMP9,MMP2,and TIMP-1 in different period of the vein bypass graft.Results: By HE and Masson staining,with the passing of modeling time,the bridge vascular collagen matrix degradation,gradually thickening of muscle fibers and the migration to the inner membrance,vascular remodeling,cause the vascular stenosis.what can be seen by immunohistochemistry is that,the animal model of NGAL,MMP9,MMP2 factor in normal venous seldom express even not express.The 14 days after the modeling of blood vessels in the membrane layer NGAL expression began to appear,membrane layer NGAL expression peaked in 30 days,and began to appear in the inner membrance.MMP9,MMP2 expression began to appear in the 7 days postoperatively,expressing a peak appeared in 14 days,after 30 days expression level tends to decline.TIMP1 expression is less in normal blood vessel walls,the 14 days after the modeling of expression peaked in vein bypass graft.Conclusions: NGAL,MMP9,MMP2 and TIMP-1 factors may be involved in the formation of early bridge vascular restenosis.NGAL as initiator,result in the expression of MMP9 and MMP2,and participate in the collagen matrix degradation and the migration of smooth muscle cells in vein bypass grafts.TIMP-1 as a negative factor,may play an important role in maintaining their own balance.