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中国临床药理学与治疗学 ›› 2006, Vol. 11 ›› Issue (8): 902-906.

• 研究原著 • 上一篇    下一篇

紫杉醇对兔血管内皮和平滑肌细胞增生影响的差异及意义

武晓静1, 葛均波, 黄岚1, 周骐1, 邹云增   

  1. 复旦大学中山医院上海市心血管病研究所, 上海 200032;
    1第三军医大学新桥医院全军心血管内科中心, 重庆 400037
  • 收稿日期:2006-03-13 出版日期:2006-08-26 发布日期:2020-11-05

Different growth response of rabbit's vascular endothelial and smooth muscle cells to Paclitaxel

WU Xiao-jing1, GE Jun-bo, HUANG Lan1, ZHOU Qi1, ZOU Yun-zeng   

  1. Shanghai Institute of Cardiovascular Disease, Zhongshan Hospital, Fudan University , Shanghai 200032 , China;
    1the Cardiovascular Center, Xinqiao Hospital , the Third Military Medical University , Chongqing 400037 , China
  • Received:2006-03-13 Online:2006-08-26 Published:2020-11-05
  • About author:WU Xiao-jing, MD, PhD, attending physician, majoring in clinical and basic research of coronary artery disease, cardiovascular pharmacology. Tel:13585676429  E-mail:xiaojingwu@21cn.com
  • Supported by:
    Supported by the National Natural Sci ence Foundation of China(No30270568;No30400517)

摘要: 目的 探讨紫杉醇对兔血管内皮和平滑肌增生影响的差异及意义。方法 将兔血管平滑肌细胞接种于共培养体系上室、内皮细胞接种于下室建立体外内膜修复模型, 观察紫杉醇对兔血管平滑肌和内皮细胞3H-TdR 掺入、细胞计数和迁移率的影响,用直线回归法计算紫杉醇对平滑肌和内皮细胞增生迁移的半数有效抑制浓度IC50结果 在1 nmol·L-1~ 1 μmol·L-1之间, 紫杉醇呈浓度依赖地抑制平滑肌细胞3H-TdR 掺入、细胞计数和迁移(n =6, P<0.01) 。在10 nmol·L-1 ~ 1 μmol·L-1 之间, 紫杉醇呈浓度依赖地抑制内皮细胞3H-TdR 掺入、细胞计数和迁移(n =6, P<0.01) 。1 nmol·L-1 紫杉醇对内皮细胞3H-TdR 掺入和细胞计数有抑制倾向, 但与对照组相比无统计学差异。而1 nmol·L-1 的紫杉醇却已显著抑制内皮细胞迁移(n =6, P<0.01) 。紫杉醇对兔血管平滑肌细胞增生、迁移抑制的IC50 分别为10.09±0.47 、9.16 ±0.54 nmol·L-1 , 对内皮细胞增生、迁移抑制的IC50分别为19.05 ±0.35 、5.37 ±0.51nmol·L-1 。10 nmol·L-1 紫杉醇作用20 min 在观察时间内能持续抑制融合内皮组平滑肌增生, 而对数内皮组平滑肌增殖在10 d 时明显高于对照组。结论 紫杉醇在抑制兔血管平滑肌细胞增生的同时也抑制内皮增生, 紫杉醇干预后平滑肌细胞增生延迟与内皮细胞再生延迟密切相关。

关键词: 紫杉醇, 平滑肌细胞, 内皮细胞, 增生, 共培养

Abstract: AIM: To investigate the effect of paclitaxel on the quantitative growth of rabbit's vascular smooth muscle cells (SMCs) and endothelial cells (ECs) and their relationshiPin vitro.METHODS: An ex vivo model of endothelium repair was developed in which rabbit's SMCs were inoculated in the upper chamber and rabbit's ECs in the lower chamber of a co-culture system.3H-TdR incorporation and cell counting were used to determine the effect of paclitaxel on the quantitative proliferation of rabbit's vascular ECs and SMCs.The migration rate was analyzed to determine the effect of paclitaxel on the migration of rabbit's vascular ECs and SMCs.The IC50 of paclitaxel on ECs and SMCs was calculated.RESULTS: The3H-TdR incorporation, cell counting and migration of rabbit's vascular SMCs were inhibited by paclitaxel of 1 nmol·L-1 -1 μmol·L-1 in a concentration-dependent manner (n =6, P<0.01).The3H-TdR incorporation and cell counting of rabbit's vascular ECs were inhibited by paclitaxel of 10 nmol·L-1 -1 μmol·L-1 andmigration by paclitaxel of 1 nmol·L-1 -1 μmol·L-1 in a concentration-dependent manner (n =6, P<0.01).The3HTdR incorporation assay resulted in the IC50 of 10.09 ±0.47 nmol·L-1 on SMCs and 19.06 ±0.35 nmol·L-1 onECs proliferation.The migration assay resulted in the IC50of 9.16 ±0.54 nmol·L-1 on SMCs and 5.37 ±0.51nmol·L-1 on ECs migration.Paclitaxel (10 nmol·L-1 ,20 min) inhibited SMCs growth of the confluent ECs grouPduring the observed period.However, increased SMCs growth was observed in the proliferative ECs grouP10 days after paclitaxel intervention.CONCLUSION: Paclitaxel inhibits not only SMCs but also ECs growth in rabbit's vascular.The delayed SMCs proliferation is closely related with the delayed ECs regeneration induced by paclitaxel.

Key words: Paclitaxel, smooth muscle cell, endothelial cell, growth, co-culture REFERENCES

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