Tumor Necrosis Factor Receptor-antibody Fusion Protein Sinus In Rat Carotid Arteryrestenosis After Ballon Injury Of Intervention

Objective Rat carotid artery neointimal hyperplasia after injury situation and recombinant human tumor necrosis factor receptor-antibody fusion protein on vascular smooth muscle cells (VSMC) proliferation cell nuclear antigen (PCNA), p53 gene expression and serum levels of tumor necrosis factor (TNF) levels of tumor necrosis factor receptor-antibody fusion protein on the balloon injury carotid artery restenosis and its mechanism. Methods Male 50 SPF SD rats (250g±50g), were randomly divided into the balloon injury group (21, including 1 week,2 weeks,4 weeks), drug intervention group (21,including 1 week,2 weeks,4 weeks), sham operation group (whichever group unaffected vascular balloon injury), each of the seven sub-group and control group (8). Rat carotid artery balloon injury model. Head Su Su-eosin staining, were observed under light microscope intimal hyperplasia; real-time fluorescence quantitative PCR (Real time RT-PCR) to detect the expression of P53 gene mRNA; enzyme-linked immunosorbent assay (Elisa) to detect serum TNF-αlevel; observed by immunohistochemistry of pro liferating cell nuclear antigen (PCNA) protein expressionResults 7 days after balloon injury, intimal thickening began, endometrial thickness increased gradually with time, the first 28 days, maximum intimal thickness; drug intervention group intimal hyperplasia than the other three groups reduced intimal VSMC and reduction of extracellular matrix; increase over time of vascular intervention group were further reduced intimal hyperplasia, intimal VSMC and extracellular matrix gradually less; in 1 week and 4 weeks the level of drug intervention group, balloon injury group, sham operation group relative expression of p53 content in the three groups compared with control group no significant change (P> 0.05); level in 2 weeks, drug intervention group relative expression of p53 was significantly higher than the other three groups (P<0.05); balloon injury, the serum levels of TNF-a significantly increased (p<0.05), with injury time increases, the level decreased gradually; peaked 1 week after injury, the difference was significant (p<0.05). After treatment the level of TNF-a decreased significantly 1 week after the intervention decreased to the lowest level, the difference was significant (p<0.05); the expression of positive signals in serum PCNA index increased significantly after balloon injury (p<0.05), with injury time increases, the level decreased gradually, reached a peak 4 weeks after injury, the difference was significant (p<0.05). After treatment the expression of PCNA index was significantly lower positive signals, the differences were significant (p<0.05). With time, its value decreased 2 weeks to reach bottom. followed by gradually increased, the difference was significant (p<0.05) Conclusion Rat carotid artery intimal hyperplasia after balloon injury significantly, PCNA protein expression increased. Tumor necrosis factor receptor-antibody fusion protein after balloon injury inhibited neointimal hyperplasia, PCNA protein expression decreased, while increased expression of P53 mRNA. Tumor necrosis factor receptor-antibody fusion protein after balloon injury inhibited neointimal hyperplasia is a possible mechanism of gene expression and down-regulated P53, PCNA expression and serum TNF-a levels.