Objective: The intimal hyperplasia caused by migration and proliferation of the smooth muscle cells play a most important role in the stenosis of the vein grafts. This study is to explore how the C myc oncogene and it...Objective: The intimal hyperplasia caused by migration and proliferation of the smooth muscle cells play a most important role in the stenosis of the vein grafts. This study is to explore how the C myc oncogene and its protein contribute to the intimal hyperplasia after the jugular vein is transplanted to the abdominal aorta and to assess the effect of Mithramycin on the intimal hyperplasia. Methods: In 60 Wistar rats, a 0.8 cm segment of the right jugular vein graft was interposed at the level of the abdominal aorta. The experiment group received Mithramycin (150 μg/kg IP) 1 h before and after the operation. The control group received normal saline, specimens of vein graft at 2 and 6 h postoperatively were subjected respectively to in situ hybridization. The vein grafts 4 weeks after operation were perfusion fixed. The specimens were stained with hemotoxylin eosin and the computer morphologic analysis system was used to evaluate the degree of intimal thickening. Immunohistochemistry studies of muscle specific α actin, C myc protein and 5 Bromodeoxyuridine were performed. Results: The areas of neointimal and the ratios of neointimal to medial area were significantly smaller and lower in the Mithramycin treated than in the control rats (P< 0.05 ). The 5 Brdu labeling rate between the two groups were also different significantly (P< 0.05 ). Muscle specific α actin showed that the smooth muscle cells formed the most area of myointimal hyperplasia. Steady state C myc mRNA level was increased from 2 h to 6 h postoperatively. The positive rate of the placebo treated group was higher significantly than that of the Mithramycin treated group (P< 0.05 ). Conclusions: Mithramycin may effectively inhibits transcription of C myc in proliferating vascular smooth muscle cells and could be useful in the prevention of restenosis after vascularization. These results support the hypothesis that systemic administration of Mithramycin might immediately prevent intimal proliferation.展开更多
文摘Objective: The intimal hyperplasia caused by migration and proliferation of the smooth muscle cells play a most important role in the stenosis of the vein grafts. This study is to explore how the C myc oncogene and its protein contribute to the intimal hyperplasia after the jugular vein is transplanted to the abdominal aorta and to assess the effect of Mithramycin on the intimal hyperplasia. Methods: In 60 Wistar rats, a 0.8 cm segment of the right jugular vein graft was interposed at the level of the abdominal aorta. The experiment group received Mithramycin (150 μg/kg IP) 1 h before and after the operation. The control group received normal saline, specimens of vein graft at 2 and 6 h postoperatively were subjected respectively to in situ hybridization. The vein grafts 4 weeks after operation were perfusion fixed. The specimens were stained with hemotoxylin eosin and the computer morphologic analysis system was used to evaluate the degree of intimal thickening. Immunohistochemistry studies of muscle specific α actin, C myc protein and 5 Bromodeoxyuridine were performed. Results: The areas of neointimal and the ratios of neointimal to medial area were significantly smaller and lower in the Mithramycin treated than in the control rats (P< 0.05 ). The 5 Brdu labeling rate between the two groups were also different significantly (P< 0.05 ). Muscle specific α actin showed that the smooth muscle cells formed the most area of myointimal hyperplasia. Steady state C myc mRNA level was increased from 2 h to 6 h postoperatively. The positive rate of the placebo treated group was higher significantly than that of the Mithramycin treated group (P< 0.05 ). Conclusions: Mithramycin may effectively inhibits transcription of C myc in proliferating vascular smooth muscle cells and could be useful in the prevention of restenosis after vascularization. These results support the hypothesis that systemic administration of Mithramycin might immediately prevent intimal proliferation.
