CAJ | 학술논문

背景:经皮冠状动脉介入治疗后再狭窄仍是影响介入治疗远期疗效的严重的临床问题.目的:在大鼠颈动脉球囊损伤模型中,探讨早期生长反应因子诱骗寡脱氧核苷酸对损伤后的血管内膜的影响,并初步探讨其分子机制.方法:利用2F Fogarty 导管损伤 Wistar 大鼠颈动脉,构建大鼠球囊损伤模型,在转染试剂 Fugene 6介导下经血管腔内转染生长反应因子诱骗寡脱氧核苷酸,苏木精-伊红染色法观察血管内膜增生情况,免疫组化法检测 Cyclin D1,观察其表达情况.结果与结论:早期生长反应因子诱骗寡脱氧核苷酸可以显著抑制大鼠颈动脉球囊损伤后血管内膜增生,同时也可以下调大鼠颈动脉球囊损伤后表达显著增加的 Cyclin D1.说明生长反应因子诱骗寡脱氧核苷酸可能通过抑制 Cyclin D1的表达,使细胞周期停滞,从而抑制损伤后的大鼠颈动脉内膜的增生.
배경:경피관상동맥개입치료후재협착잉시영향개입치료원기료효적엄중적림상문제.목적:재대서경동맥구낭손상모형중,탐토조기생장반응인자유편과탈양핵감산대손상후적혈관내막적영향,병초보탐토기분자궤제.방법:이용2F Fogarty 도관손상 Wistar 대서경동맥,구건대서구낭손상모형,재전염시제 Fugene 6개도하경혈관강내전염생장반응인자유편과탈양핵감산,소목정-이홍염색법관찰혈관내막증생정황,면역조화법검측 Cyclin D1,관찰기표체정황.결과여결론:조기생장반응인자유편과탈양핵감산가이현저억제대서경동맥구낭손상후혈관내막증생,동시야가이하조대서경동맥구낭손상후표체현저증가적 Cyclin D1.설명생장반응인자유편과탈양핵감산가능통과억제 Cyclin D1적표체,사세포주기정체,종이억제손상후적대서경동맥내막적증생.
BACKGROUND: Restenosis fol owing percutaneous coronary intervention is stil a clinical y serious problem which negatively affects the long-term therapeutic benefit of percutaneous coronary intervention. OBJECTIVE: To investigate the effect of Egr-1 decoy oligodeoxynucleotides via intracerebroventricular injection on the neointima after carotid bal oon injury and to primarily study its mechanism of inhibiting neiointimal hyperplasia, thus providing a new prospect to find a new target of vascular remodeling and restenosis. METHODS: Endothelial denuded carotid models were prepared in rats by bal oon withdrawal injury with the help of 2F Fogarty. Then Egr-1 decoy oligodeoxynucleotides were injected into injured vascular subsection which was mediated by Fugene6 transfection reagent. The extent of neointimal hyperplasia and the expression of Cyclin D1 were detected by hematoxylin-eosin staining and immunohistochemistry, respectively.RESULTS AND CONCLUSION: Neointimal hyperplasia was significantly inhibited by Egr-1 decoy oligodeoxynucleotides. The expression of Cyclin D1, which was dramatical y increased after bal oon injury of rat common carotid artery, was significantly down-regulated by Egr-1 decoy oligodeoxynucleotides. Egr-1 decoy oligodeoxynucleotides may inhibit neointimal hyperplasia fol owing bal oon injury of rat common carotid artery via down-regulation of Cyclin D1.