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普伐他汀和粒细胞集落刺激因子对心肌缺血小鼠内皮祖细胞动员的影响

[Effects of pravastatin and granulocyto-colony stimulating factor in mobilizing endothelial progenitor cells in mice with myocardial ischemia].

作者信息

Chen Ting-ting, Mi Wei-dong, Wang Gang, Li Li-bing, Gao Chang-qing

机构信息

Department of Cardiovascular Surgery, General Hospital of PLA, Beijing 100853, China. chentt301 @263.com

出版信息

Nan Fang Yi Ke Da Xue Xue Bao. 2009 Aug;29(8):1660-2.

Abstract

OBJECTIVE

To compare the effects of pravastatin and granulocyto-colony stimulating factor (G-CSF) in mobilizing endothelial progenitor cells (EPCs) in mice with myocardial ischemia, and explore the possible mechanism of EPC mobilization.

METHODS

Ninety-six mice were randomly divided into 4 groups (n=24), namely the control group, saline group, pravastatin group and G-CSF group. In the latter 3 groups, myocardial ischemia was induced with isoprenine followed by intraperitoneal injections of normal saline, pravastatin and G-CSF for 5 consecutive days. On days 1, 5, 7, and 9 after establishment of myocardial ischemia, 6 mice from each group were randomly selected for measurement of the EPC count and serum concentrations of vascular endothelial growth factor (VEGF).

RESULTS

Compared with the control group, EPC count increased slightly in the saline group on days 1, 5, and 7. EPC count increased significantly in pravastatin group on days 5, 7 and 9 in comparison with that of the saline group, and the increment was more obvious in G-CSF group. In comparison with the control group, the concentrations of VEGF augmented on days 5, 7 and 9 in the order of saline group, pravastatin group and G-CSF group. The effect of G-CSF on EPC mobilization was positively correlated to VEGF concentrations.

CONCLUSION

Myocardial ischemia induces EPC mobilization and VEGF release. Both Pravastatin and G-CSF can enhance EPC mobilization from the bone marrow and VEGF release, but G-CSF produces a stronger effect on EPC mobilization in association of VEGF release.

摘要

目的

比较普伐他汀和粒细胞集落刺激因子(G-CSF)对心肌缺血小鼠内皮祖细胞(EPCs)动员的影响,并探讨EPCs动员的可能机制。

方法

将96只小鼠随机分为4组(n = 24),即对照组、生理盐水组、普伐他汀组和G-CSF组。后3组用异戊二烯诱导心肌缺血,随后连续5天腹腔注射生理盐水、普伐他汀和G-CSF。在心肌缺血建立后的第1、5、7和9天,每组随机选取6只小鼠测量EPC计数和血管内皮生长因子(VEGF)的血清浓度。

结果

与对照组相比,生理盐水组在第1、5和7天EPC计数略有增加。与生理盐水组相比,普伐他汀组在第5、7和9天EPC计数显著增加,G-CSF组增加更明显。与对照组相比,VEGF浓度在第5、7和9天按生理盐水组、普伐他汀组和G-CSF组的顺序升高。G-CSF对EPC动员的作用与VEGF浓度呈正相关。

结论

心肌缺血诱导EPC动员和VEGF释放。普伐他汀和G-CSF均可增强骨髓EPC动员和VEGF释放,但G-CSF在VEGF释放方面对EPC动员产生更强的作用。

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