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粒细胞集落刺激因子促进超声微泡破坏诱导的血管生成。

Granulocyte colony-stimulating factor facilitates the angiogenesis induced by ultrasonic microbubble destruction.

作者信息

Miyake Yuichi, Ohmori Koji, Yoshida Junji, Ishizawa Makoto, Mizukawa Mizuki, Yukiiri Kazushi, Kohno Masakazu

机构信息

Division of Cardiology, Department of Cardiorenal Cerebrovascular Medicine, Kagawa University School of Medicine, Kagawa, Japan.

出版信息

Ultrasound Med Biol. 2007 Nov;33(11):1796-804. doi: 10.1016/j.ultrasmedbio.2007.05.017. Epub 2007 Aug 8.

Abstract

Ultrasonic destruction of microbubbles (US/MB) in the microcirculation causes local inflammatory cell infiltration, which has been shown to induce angiogenesis. Granulocyte colony-stimulating factor (G-CSF), which mobilizes myelomonocytic cells from the bone marrow and enhances vascular endothelial growth factor (VEGF) release from these cells, has also been applied to therapeutic angiogenesis induction. In the present study, we sought to examine the potential of G-CSF pretreatment to enhance the angiogenic effect of US/MB. Ischemic hindlimbs in mice were treated with either a predetermined minimal effective dose (300 mug/kg) of G-CSF, US/MB alone or G-CSF pretreatment followed by US/MB at seven days after removal of the femoral artery. Ultrasonic destruction of microbubbles was performed as intermittent pulsed local insonation using a diagnostic ultrasound scanner at a peak negative pressure of 1.4 MPa after intravenous injection of perfluorocarbon microbubbles. At 21 days after the treatment, we quantified the surface vascularity using a grid method and the capillary density using an alkaline phosphatase stain. Relative to the capillary density in normal muscle, the capillary density in the treated limbs was restored to 74 +/- 13% by G-CSF alone and 90 +/- 20% by US/MB alone (p < 0.05 vs. both untreated and G-CSF alone), and further increased to 101 +/- 21% by G-CSF pretreatment. The collateral growth induced by the combination of G-CSF pretreatment and US/MB was 2.8- and 1.4-fold greater than the growth induced by G-CSF alone and US/MB alone, respectively (p < 0.05 for both). Thus, pretreatment with a single minimal effective dose of G-CSF can augment the angiogenic effect of US/MB.

摘要

微循环中微泡的超声破坏(US/MB)会引起局部炎性细胞浸润,这种浸润已被证明可诱导血管生成。粒细胞集落刺激因子(G-CSF)可从骨髓中动员髓单核细胞,并增强这些细胞释放血管内皮生长因子(VEGF),也已被应用于诱导治疗性血管生成。在本研究中,我们试图研究G-CSF预处理增强US/MB血管生成作用的潜力。在切除股动脉7天后,对小鼠缺血后肢分别给予预定的最小有效剂量(300μg/kg)的G-CSF、单独的US/MB或G-CSF预处理后再进行US/MB处理。静脉注射全氟碳微泡后,使用诊断超声扫描仪以1.4MPa的峰值负压进行间歇性脉冲局部超声照射,以实现微泡的超声破坏。治疗21天后,我们使用网格法对表面血管密度进行定量,并使用碱性磷酸酶染色对毛细血管密度进行定量。相对于正常肌肉中的毛细血管密度,单独使用G-CSF可使治疗后肢的毛细血管密度恢复至74±13%,单独使用US/MB可使其恢复至90±20%(与未治疗组和单独使用G-CSF组相比,p<0.05),而G-CSF预处理可使其进一步增加至101±21%。G-CSF预处理与US/MB联合诱导的侧支生长分别比单独使用G-CSF和单独使用US/MB诱导的生长大2.8倍和1.4倍(两者p<0.05)。因此,单次最小有效剂量的G-CSF预处理可增强US/MB的血管生成作用。

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