摘要
目的 :探讨球囊损伤血管内皮后平滑肌细胞 (SMC)凋亡的机制。方法 :采用末端脱氧核苷酸转移酶介导的三磷酸脱氧尿嘧啶缺口末端标记法 (TUNEL)和免疫组织化学技术检测球囊损伤内皮后血管平滑肌细胞 (VSMC)凋亡及Bax、Bcl- 2蛋白的变化。结果 :球囊损伤内皮后第 3d ,血管中层出现凋亡的SMC ;损伤后第 7d ,内膜和中层SMC凋亡率最高 ,凋亡的SMC主要分布在内膜层 ;以后逐渐降低 ,至损伤后第 2 8d ,仅内膜层有少量凋亡的SMC。Irbesartan显著增加SMC凋亡 (P <0 0 1)。球囊损伤内皮后第 3d ,血管中层Bax、Bcl- 2表达显著高于假手术组 (P <0 0 1) ;损伤后第 7d血管中Bax表达最高 ,是假手术组的 3倍 ,以后表达减少。球囊损伤内皮后Bcl- 2表达逐渐增多 ,至第 2 8d表达最高。Bax/Bcl- 2也在损伤后第 7d达最高 ,至第 2 8d降至基础水平以下。Irbesartan使Bax表达增高、Bcl- 2表达降低、Bax/Bcl- 2升高。结论 :Bax、Bcl- 2参与了球囊损伤内皮后VSMC凋亡的调节。
AIM: To investigate the mechanism of vascular smooth muscle cells (VSMC) apoptosis after balloon injury. METHODS: VSMCs apoptosis, Bax protein and Bcl-2 protein was measured by terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL) and immunohistochemical technique after balloon injury.RESULTS: VSMCs apoptosis occurred in vascular media at 3 days after balloon injury and reached a peak in media and intima where apoptosis was mainly present at 7 days, then decreased. At 28 days after balloon injury, only a few apoptosis cells were in intima. Irbesartan significantly increased VSMCs apoptosis ( P<0.01 ). Expressions of Bax and Bcl-2 were significantly higher in vascular media at 3 days after balloon injury than sham( P<0.01 ). At 7 days, Bax expression reached a peak which was three times as that of sham, and then decreased. After balloon injury, Bcl-2 expression was generally increased and reached its peak at 28 days. The ratio of Bax to Bcl-2 (Bax/Bcl-2) also reached its peak at 7 days and was decreased under basal level at 28 days. Irbesartan increased Bax and the ratio of Bax to Bcl-2, while decreased Bcl-2. CONCLUSION: Bcl-2 and Bax contribute to the regulation of VSMC apoptosis after balloon injury.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2000年第8期694-697,I001,共4页
Chinese Journal of Pathophysiology
