摘要
目的 观察XS0 6 0 1(由川芎和赤芍的有效部位组成 )对猪冠状动脉球囊损伤后细胞凋亡及相关基因bcl 2、野生型p5 3表达的影响。方法 球囊扩张损伤猪冠状动脉左前降支 (LAD)中段内膜的方法建立再狭窄 (RS)模型。其中对照组不给予特殊药物治疗 ,各药物组于术前 2天开始给药 ,持续至术后 4周处死。原位杂交方法观察球囊损伤后内膜中bcl 2、p5 3mRNA表达 ,原位末端标记法(ISEL)检测内膜中的凋亡细胞 ,并研究药物对细胞凋亡的影响。结果 损伤后 4周动脉在内弹力板(IEL)断裂情况下 ,形成了明显的新生内膜。小剂量和大剂量XS0 6 0 1均可增加内膜中的凋亡细胞 ,其凋亡细胞阳性表达面积率与对照组相比差异有显著性 (P <0 0 1和P <0 0 5 ) ;并能减少内膜中的bcl 2阳性杂交颗粒 ,增加p5 3阳性杂交颗粒。结论 猪冠状动脉球囊损伤后新生内膜中的细胞凋亡水平较低 ,凋亡抑制基因bcl 2的表达增加。XS0 6 0 1可通过减少凋亡抑制基因bcl 2的表达 ,上调凋亡促进基因p5 3的表达 ,从而对猪冠状动脉球囊损伤后SMC增殖过程中较低的凋亡水平进行调控 ,诱导新生内膜中的细胞凋亡。
Objective To investigate the effect of XS0601 (consisting of active position of Ligusticum chuanxiong Hort and Paeonia lactiflora Pall) on apoptosis and expression of apoptosis related gene bcl 2 and wild type p53 in neointima of porcine coronary artery after balloon injury Methods Restenosis model was established by oversized balloon injury at mid region of the left anterior descending (LAD) coronary arteries on swine Treated animals (administering drugs 2 days before balloon injury and continuing until the swine were killed 4 weeks after balloon injury) were compared with control animals receiving balloon injury alone Expression of p53 and bcl 2 mRNA were analyzed with in situ hybridization Apoptosis was detected with in situ end labeling (ISEL) Results Four weeks after coronary angioplasty, obvious neointima formed based on fracture of internal elastic lamina (IEL) Low dose and high dose XS0601 could both increase proportion of apoptosis positive area compared with control group ( P <0 05, P <0 01) Besides, XS0601 could also reduce expression of bcl 2 mRNA and increase expression of p53 mRNA Conclusion Increased expression of bcl 2 mRNA (apoptosis inhibiting gene) and decreased apoptosis level were found in neointima of coronary artery after balloon dilation XS0601 could downregulate expression of bcl 2 mRNA and upregulate wild type p53 mRNA (apoptosis inducing gene), thus induce apoptosis in neointima
出处
《中国介入心脏病学杂志》
2001年第3期152-154,共3页
Chinese Journal of Interventional Cardiology
基金
国家"九.五"攻关课题的部分内容 (No 96 90 6 0 6 0 1)
