Research of nuclear factor-κB siRNA to prevent proliferation and restenosis of vein grafts
Sun Wen-yu
Abstract
Sun Wen-yu
Abstract
Objective To investigate the effects of nuclear factor κB small interfering RNA ( NF-κB siRNA) on intimal proliferation and expressions of inflammatory factors in autologous vein grafts. Methods A total of 80 male Wistar rats ( weight,300 g to 350 g) were randomly divided into four groups: 1) Group A( n =10) ,normal group without transplantation; 2) Group B( n = 18) ,vein transplantation only; 3) Group C ( n = 26) ,vein transplantation but the graft was processed by blank plasmid liposome complexes; 4) Group D( n = 26) ,vein transplantation but the graft was transfected by NF-κB siRNA liposome complexes. The transplantation was to replace an abdominal aortic vein with the autologous right external jugular vein. At four time points ( 3rd ,7th,14th,21st day) ,autografts were processed to determine intima hyperplasia,PCNA,M CP-1 mRNA,TNF-α mRNA and NF-κB p65 protein. Results Intimal hyperplasia and VSM C obviously proliferated in groups B,C and D. At the 3rd day,expressions of M CP-1 mRNA and TNF-α mRNA in group D was significantly lower than group C ( P 0. 05) . At the 7th day,the levels of NF-κB p65 protein in group B and C were significantly higher than in group A ( P 0. 05) . Compared with group C,the levels of NF-κB p65 protein in group D were lower( P 0. 05) . Conclusion Expressions of M CP-1 mRNA and TNF-α mRNA have some relationships with NF-κB p65 protein. The proliferation of vascular endothelial cells and expression of inflammatory cytokines are changing and correlative in the vein graft. Transfection of NF-ΚB siRNA liposome complexes on the autologous vein graft can inhibit its proliferation and reduce expressions of NF-κB,M CP-1 and TNF-α.
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Objective To investigate the effects of nuclear factor κB small interfering RNA ( NF-κB siRNA) on intimal proliferation and expressions of inflammatory factors in autologous vein grafts. Methods A total of 80 male Wistar rats ( weight,300 g to 350 g) were randomly divided into four groups: 1) Group A( n =10) ,normal group without transplantation; 2) Group B( n = 18) ,vein transplantation only; 3) Group C ( n = 26) ,vein transplantation but the graft was processed by blank plasmid liposome complexes; 4) Group D( n = 26) ,vein transplantation but the graft was transfected by NF-κB siRNA liposome complexes. The transplantation was to replace an abdominal aortic vein with the autologous right external jugular vein. At four time points ( 3rd ,7th,14th,21st day) ,autografts were processed to determine intima hyperplasia,PCNA,M CP-1 mRNA,TNF-α mRNA and NF-κB p65 protein. Results Intimal hyperplasia and VSM C obviously proliferated in groups B,C and D. At the 3rd day,expressions of M CP-1 mRNA and TNF-α mRNA in group D was significantly lower than group C ( P 0. 05) . At the 7th day,the levels of NF-κB p65 protein in group B and C were significantly higher than in group A ( P 0. 05) . Compared with group C,the levels of NF-κB p65 protein in group D were lower( P 0. 05) . Conclusion Expressions of M CP-1 mRNA and TNF-α mRNA have some relationships with NF-κB p65 protein. The proliferation of vascular endothelial cells and expression of inflammatory cytokines are changing and correlative in the vein graft. Transfection of NF-ΚB siRNA liposome complexes on the autologous vein graft can inhibit its proliferation and reduce expressions of NF-κB,M CP-1 and TNF-α.
Key concepts: Intimal hyperplasia, Transplantation, Restenosis, Messenger RNA, Group A, Group B, Hyperplasia, Medicine