血管内皮生长因子预防血管成形术后再狭窄的机理
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The Mechanical Study of Vascular Endothelial Growth Factor on the Prevention of Restenosis after Angioplasty
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    摘要:

    为探讨血管内皮生长因子预防血管成形术后再狭窄的机理,构建含人血管内皮生长因子165基因的重组腺病毒,感染体外培养的血管平滑肌细胞,将人脐静脉内皮细胞和血管平滑肌细胞分别分成对照组、H2 O2 处理组和H2 O2 +血管内皮生长因子处理组,采用WST 1比色法、原位末端标记法及流式细胞术检测各组细胞光密度值和凋亡发生情况。结果发现,人脐静脉内皮细胞中,与对照组和H2 O2 +血管内皮生长因子处理组比较,H2 O2 处理组光密度值降低,凋亡细胞明显增加;血管平滑肌细胞中上述改变相反。提示H2 O2 能促进平滑肌细胞增殖,诱导内皮细胞凋亡,抑制内皮细胞增殖及平滑肌细胞凋亡,促进再狭窄的发生,而血管内皮生长因子能拮抗H2 O2 的作用,有利于再狭窄的防治,为血管内皮生长因子预防再狭窄提供新的理论依据

    Abstract:

    Aim To evaluate the mechanism of vascular endothelial growth factor (VEGF) on prevention of restenosis after angioplasty. Methods The recombinant adenovirus containing the cDNA for hVEGF165 was constructed and infected vascular smooth muscle cell(VSMC)in vitro. 72 hours after the infection the conditioned medium containing VEGF was collected. Then the VSMC and human umbilical vein endothelial cell(hUVEC) were divided into control group,H 2O 2 treated group and H 2O 2+VEGF treated group to observe the proliferation and apoptosis by WST-1 method,TUNEL and FCM. Results To hUVEC,the OD value wasless frequent in the H 2O 2 treated group than that in the control and H 2O 2+VEGF treated group,the apoptosis was markedly superior in H 2O 2 treated group compared with control and H 2O 2 + VEGF-treated group. To VSMC,the changes of OD value and apoptosis were contrary to hUVEC. Conclusions H 2O 2 stimulated the proliferation of VSMC and induced the apoptosis of hUVEC, inhibited the proliferation of hUVEC and the apoptosis of VSMC, improved the restenosis. VEGF inhibited the effect of H 2O 2 on hUVEC and VSMC, and prevented restenosis. These results offered further theoretical evidence for VEGF on the prevention of restenosis after angioplasty.

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刘启功,陆再英,周洪莲,张卫东,颜进.血管内皮生长因子预防血管成形术后再狭窄的机理[J].中国动脉硬化杂志,2001,9(3):209~212.

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  • 收稿日期:2000-10-30
  • 最后修改日期:2001-04-19
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