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目的 探讨血管球囊损伤后平滑肌细胞 (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后血管平滑肌细胞凋亡及血管紧张素Ⅱ 1型受体 (AT1 R)表达的变化。结果 球囊损伤后第 3天 ,血管中层AT1 R表达比假手术组显著增多 (P <0 0 5 ) ,以后无显著改变 ;损伤后第 7天内膜层AT1 R为中层的近 2倍 ;至损伤后第 2 8天 ,内膜层AT1 R表达最高 ;球囊损伤后第 3天 ,血管中层出现凋亡的SMC ;损伤后第 7天 ,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 8天 ,仅内膜层有少量凋亡的SMC ,AT1 R拮抗剂Irbesartan显著增加SMC凋亡。结论 血管球囊损伤后 ,AT1 R上调 ,血管紧张素Ⅱ通过与AT1 R结合抑制VSMC凋亡。
Objective To investigate the mechanism of apoptosis of vascular smooth muscle cells (SMC) after vascular balloon injury. Methods TUNEL and immunohistochemical techniques mediated by terminal deoxynucleotidyl transferase were used to detect the apoptosis of vascular smooth muscle cells and the expression of angiotensin Ⅱ type 1 receptor (AT1 R) expression changes. Results On the third day after balloon injury, the expression of AT1 R in the middle layer of blood vessel was significantly increased (P <0.05), but no significant change was observed after the balloon injury. The AT1 R in the middle layer of the balloon was almost 2 times higher on the 7th day after balloon injury. At day 28 after injury, the expression of AT1 R in intima layer was the highest. At 3 days after balloon injury, apoptotic SMCs appeared in the middle layer of balloon injury. On the 7th day after injury, the apoptosis rate of intima and middle SMC was highest and apoptosis SMC mainly distributed in the intima layer; then gradually decreased to the 28th day after the injury, only a small amount of endometrial apoptosis SMC, AT1 R antagonist Irbesartan significantly increased SMC apoptosis. Conclusion After vascular balloon injury, AT1 R is upregulated. Angiotensin Ⅱ inhibits VSMC apoptosis through binding to AT1 R.