摘要
目的探讨粒细胞集落刺激因子（G—CSF）治疗对川崎病小鼠模型内皮祖细胞（EPC）数量和功能以及冠状动脉损伤的影响。方法采用酪乳杆菌细胞壁提取物（LCWE）单次腹腔注射的方法制备川崎病C57BL／6小鼠模型。48只小鼠以随机数字表法分为3组：模型组、G-CSF治疗组及对照组（磷酸盐缓冲液腹腔注射），每组16只。于实验的第5～9天应用重组人G．CSF对其进行治疗。对循环EPC数量及骨髓EPC功能进行检测，同时观察其冠状动脉损伤的改善情况。结果模型组于实验的第14天，冠状动脉主干周围可以见到大量炎细胞浸润，其外周血中循环EPC含量[（0．017±0．008）％]明显低于对照组[（0．028±0．007）％]（t=2．037，P〈0．05），56d冠状动脉弹力层的破坏清晰可见，其循环EPC含量[（0．016±0．007）％]仍低于对照组（t=2．575，P均〈0．05）。治疗组于实验的第14天，冠状动脉主干周围同样可见炎细胞浸润，而其循环EPC含量[（0．042±0．015）％]较模型组高（t=4．629，P〈0．05），第56天，循环EPC含量[（0．029±0．012）％]仍高于模型组（t=2．789，P〈0．05），同时，冠状动脉弹力层也没有发生显著的破坏。骨髓EPC的体外功能检测显示，模型组小鼠骨髓EPC体外增殖、黏附和迁移能力均低于对照组。而治疗组EPC的功能均较模型组明显上调（P〈0．01），且与对照组比较，差异无统计学意义（P〉0．05）。结论G—CSF能够通过上调EPC数量和功能，从而达到阻止JiI崎病小鼠模型冠状动脉损伤发生的目的。
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. easei 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 downregulated compared to controls [ （ 3. 1 ±0. 6） cells/HPF and （ 3. 3 ± 0. 6 ） cells/HPV 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] fu
出处
《中华儿科杂志》
CAS
CSCD
北大核心
2012年第10期788-792,共5页
Chinese Journal of Pediatrics
关键词
川崎病
小鼠
粒细胞集落刺激因子
内皮祖细胞
Kawasaki disease
Mice
Granulocyte colony-stimulating factor
Endothelial progenitor cell
