摘要
目的：探讨去纤酶抑制血管损伤后内膜增生的机制。方法：以犬冠状动脉内植入过大钽丝支架致血管内膜过度增生为动物模型，用常规组织方法、免疫组化及ｍＲＮＡ原位杂交技术分别检测新生内膜厚度、新生内膜中血管平滑肌细胞增生及Ｃ－ｆｏｓ基因的转录情况，并采用随机对照方法观察去纤酶对血管损伤后内膜增生程度、α平滑肌肌动蛋白表达及Ｃ－ｆｏｓ基因转录的影响。结果：去纤酶组新生内膜厚度、α平滑肌肌动蛋白的表达及Ｃ－ｆｏｓ的转录水平均显著低于对照组（Ｐ分别＜０．０５及０．０１）。结论：去纤酶可能通过影响Ｃ－ｆｏｓ基因的转录水平而抑制血管平滑肌细胞增生。
Objective:To investigate the mechanism of defibrase inhibiting the neointimal proliferation after vascular injury. Methods: Oversized tantalum coils were implanted into coronary arteries in 19 dogs. Ten dogs were randomly treated with defibrase (group A) and the others (group B) received two doses of heparin only. The dogs were killed 28 days after the implantation. Histopathology with hematoxylin eosin staining, immunohistochemisty with α Actin monocolon antibody and in situ hybridization were employed to investigate the neointimal and to detect the proliferation of vascular muscle cells and the expression of C fos oncogene. A computer image analysis system was used to measure the neointimal thickness and the stain density indexes of α Actin and C fos. Results:The neointimal thickness, the expression of α Actin and the transcription of C fos oncogene were lower in group A than in group B. Conclusion:Defibrase decreased the intimal hyperplasia, which might be the results of inhibiting the proliferation of vascular muscle cells by decreasing the expression of C fos oncogene.
出处
《军医进修学院学报》
CAS
1999年第1期57-58,共2页
Academic Journal of Pla Postgraduate Medical School
基金
"八五"军队医药卫生科研基金
