摘要
目的 :探讨动脉内膜损伤后狭窄的发生机制。方法 :用 2 4只新西兰大白兔建立腹主动脉下端内膜损伤后狭窄模型 ,采用原位末端标记法 (TUNEL)、免疫组化和原位杂交方法 ,检测增殖内膜中血管平滑肌 (VSMCs)增殖、凋亡及相关基因c fos、c myc、p5 3和PCNA的表达。 结果 :术后 1～ 2周PCNA达到高峰 ,与 4周～ 12周组间差异有显著性 (P <0 0 5 ) ,TUNEL在术后4个月内保持低水平 ,损伤后 4个月内VSMCs凋亡低于增殖水平。术后 1～ 2周 ,c fos、c mycmRNA表达强阳性 ,在 3个月后未见表达。p5 3只在 1周内有弱阳性而其余各时间点未见表达。 结论 :VSMCs增殖和凋亡的失衡与动脉内膜损伤后狭窄密切相关 ,c fos和c myc参与了VSMCs凋亡和增殖的调节 。
purpose To study the mechanism of arterial intimal stenosis. Methods Stenosis models of ventral aorta after arterial intimal injur were established in 24 rabbits. TUNEL and immunohistochemistry and in situ hybridization were used to detect the expression of apoptosis and proliferation related gene c fos, c myc and p53 and proliferation cell nuclear antigen (PCNA) of smooth muscle cell (SMC) in injuryed intimae. Results From 1 to 2 weeks, the expression of PCNA reached its peak value that was different from the group of 4 to 12 weeks ( P <0 05). The level of TUNEL was low in the period of 1 week to 4 months. Intimal proliferation was accompanied with lower rate of apoptosis. The results of in situ hybridization showed that SMCs of neointima in the 1～2 weeks group displayed intense c myc, c fos mRNA staining,and no positivity after 3 months. But p53 staining was slightly positive only in the first week. Conclusions The imbalance of apoptosis and proliferation may be related to the restenosis after arterial intimal injury. c myc and c fos may involve in the regulate of apoptosis and proliferation of VSMCs. Adopting the mixed strategy to regulation the balance between apoptosis and proliferation may be useful to prevent arterial intimal stenosis.
出处
《临床与实验病理学杂志》
CAS
CSCD
2002年第1期76-78,共3页
Chinese Journal of Clinical and Experimental Pathology
基金
江苏省教育厅自然科学基金 (No 98KJB3 10 0 0 2 )
关键词
动脉内膜损伤
血管损伤
平滑肌
基因表达
兔
细胞增殖
细胞凋亡
arteries
tanica intima injuries
muscle,smooth,vascular
proliferation
apoptosis
gene expression
rabbits
