[粒细胞集落刺激因子对川崎病小鼠模型冠状动脉病变中内皮祖细胞的影响]
[Effect of granulocyte colony-stimulating factor on endothelial progenitor cell for coronary artery lesion in Kawasaki disease mice model].
作者信息
Chen Zhi, Liu Jun-feng, DU Zhong-dong, Wan Sui-gui, Guan Yun-qian
机构信息
Department of Cardiology, Beijing Children's Hospital, Capital Medical University, Beijing 100045, China.
出版信息
Zhonghua Er Ke Za Zhi. 2012 Oct;50(10):788-92.
OBJECTIVE
Number and function of endothelial progenitor cell (EPC) and coronary artery lesion in Kawasaki disease (KD) model were evaluated to investigate therapeutic efficacy of granulocyte colony-stimulating factor (G-CSF).
METHOD
C57BL/6 mice were injected with L. casei cell wall extract (LCWE); 48 mice were divided into 3 groups randomly: KD model group; G-CSF treated model group and control group, 16 in each. G-CSF was subcutaneously injected from day 5 to day 9 after injection of LCWE. Coronary artery lesion, number of circulating EPC and the function of bone marrow EPC were evaluated.
RESULT
In model group, inflammatory infiltration was found around coronary artery at 14 days. The number of circulating EPC was significantly decreased in model group (0.017% ± 0.008%) compared to control (0.028% ± 0.007%) (t = 2.037, P < 0.05). Disruption of elastin was consistently observed at 56 days. Stimulated by G-CSF, inflammatory infiltration was found around the coronary artery at day 14, while the number of circulating EPC (0.042% ± 0.015%) was increased significantly compared to models (t = 4.629, P < 0.05). At the day 56, the number of circulating EPC was decreased slightly (0.029% ± 0.012%), but still higher than the model group (t = 2.789, P < 0.05), and have no significant difference compared to controls (P > 0.05). Furthermore, there was no elastin disruption in the G-CSF group. In model group, bone marrow EPC's proliferation ability of absorbance (A value) was 0.38 ± 0.09 in thiazolyl blue assay, less than controls (0.61 ± 0.14, P < 0.01). Adhesion and migration function were down-regulated compared to controls [(3.1 ± 0.6) cells/HPF and (3.3 ± 0.6) cells/HPF vs. (6.4 ± 1.2) cells/HPF and (6.2 ± 0.5) cells/HPF, both P < 0.01]. In the G-CSF treated group, proliferation ability (A 0.58 ± 0.10), adhesion [(6.17 ± 1.13) cells/HPF], migration [(6.29 ± 0.42) cells/HPF] function were increased significantly compared to the model group (P < 0.01).
CONCLUSION
G-CSF can up-regulate EPC number and function to prevent coronary artery lesion in mice model of KD.
目的
评估川崎病（KD）模型中内皮祖细胞（EPC）的数量和功能以及冠状动脉病变情况，以研究粒细胞集落刺激因子（G-CSF）的治疗效果。
方法
将C57BL/6小鼠注射干酪乳杆菌细胞壁提取物（LCWE）；48只小鼠随机分为3组：KD模型组；G-CSF治疗模型组和对照组，每组16只。在注射LCWE后第5天至第9天皮下注射G-CSF。评估冠状动脉病变、循环EPC数量及骨髓EPC功能。
结果
模型组在14天时冠状动脉周围出现炎症浸润。模型组循环EPC数量（0.017%±0.008%）与对照组（0.028%±0.007%）相比显著降低（t=2.037，P<0.05）。在56天时持续观察到弹性蛋白破坏。经G-CSF刺激，14天时冠状动脉周围出现炎症浸润，而循环EPC数量（0.042%±0.015%）与模型组相比显著增加（t=4.629，P<0.05）。在56天时，循环EPC数量略有下降（0.029%±0.012%），但仍高于模型组（t=2.789，P<0.05），与对照组相比无显著差异（P>0.05）。此外，G-CSF组未出现弹性蛋白破坏。在模型组，噻唑蓝法检测骨髓EPC的增殖能力吸光度（A值）为0.38±0.09，低于对照组（0.61±0.14，P<0.01）。与对照组相比，黏附及迁移功能下调[（3.1±0.6）个细胞/高倍视野和（3.3±0.6）个细胞/高倍视野对（6.4±1.2）个细胞/高倍视野和（6.2±0.5）个细胞/高倍视野，均P<0.01]。在G-CSF治疗组，增殖能力（A 0.58±0.10）、黏附[（6.17±1.13）个细胞/高倍视野]、迁移[（6.29±0.42）个细胞/高倍视野]功能与模型组相比显著增加（P<0.01）。
结论
G-CSF可上调EPC数量和功能，预防KD小鼠模型中的冠状动脉病变。
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