期刊文献+

细胞凋亡在原发性下肢深静脉功能不全的大隐静脉曲张发病中的作用 被引量:10

Effect of apoptosis in the pathogenesis of the great saphenous varicose result ing from primary deep venous insufficiency
下载PDF
导出
摘要 目的 探讨细胞凋亡在原发性下肢深静脉功能不全 (PDVI)的大隐静脉曲张发病中的作用。方法 采用透射电镜、电泳、原位DNA片段末端标记 (TUNEL )和免疫组织化学法检测原发性下肢深静脉功能不全的大隐静脉第一对瓣窦细胞凋亡及相关基因Bcl 2的表达。结果 试验组 (PDVI)3 8例 ,正常对照组 5例。试验组大隐静脉第一对瓣膜平均细胞凋亡数 6.3 0± 2 .70 ,平均细胞凋亡率 0 .42± 2 .12 ,Bcl 2平均阳性率 0 .2 9± 1.80 ;试验组的细胞凋亡数和细胞凋亡率均明显高于对照组 (分别为 1.60± 0 .81和 0 .2 1± 1.10 ) ,差异有显著性 (均为P <0 .0 5)。试验组大隐静脉反流程度为I° ,II°者细胞凋亡率 (3 .0 6± 1.65)明显低于III° ,IV°者 (9.85± 2 .3 6) (P <0 .0 5)。试验组深静脉第一对瓣膜Bcl 2表达明显低于对照组 (0 .3 5± 1.0 3 ) (P >0 .0 5)。结论 细胞凋亡及Bcl ObjectiveTo study the effect of apoptosis in the p athogenesis of great saphenous varicose(GSV) resulting from primary deep ven ous insufficiency (PDVI). Methods Apoptosis and Bcl-2 expres sion in the segment of first valve sinus of the GSV of PDVI of lower limbs w ere detected by transmission electron microscopy(TEM), agarose gel electrophore sis, TUNEL and immunohistochemistry. ResultsThere were 38 case s of PDVLs in experment group and 5 normal GSV in control group. In experiment group,the apoptosis cells(AC) (6.30± 2.70 )and apoptosis rate (AR)(0.42±2 .12) in the first valve sinus of GSV were significantly higher than those in control group(1.60±0.81,0.21±1.10,respectively)(all P<0.05).In patients wi th I°,II° blood reflux of deep venous ,the AC(3.06±1.65)and AR(0.36±2.41) were significantly lower than those in patients with III°,IV° blood reflux(9. 85±3.26,0.48±2.96,respectively)(all P<0.05).The Bcl-2 expressions in the segment of first valve sinus of GSV in patient with PDVI (0.29±1.80) was significantly lower than that in control group (0.3 5± 1.03 )(P<0.05). ConclusionsApoptosis and suppressi on of Bcl-2 expression have important roles in the pathogenesis of PDVI of lower extremities.
出处 《中国普通外科杂志》 CAS CSCD 2004年第1期25-28,共4页 China Journal of General Surgery
基金 国家自然科学基金资助项目(39870 80 0 )
关键词 静脉机能不全 病因学 静脉曲张 细胞凋亡 VENOUS INSUFFIC IENCY/etiol VARICOSE VEINS/etiol APOPT OSIS
  • 相关文献

参考文献1

二级参考文献3

共引文献21

同被引文献161

引证文献10

二级引证文献89

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部