Administration of Granulocyte Colony-Stimulating Factor Ameliorates Radiation-Induced Hepatic Fibrosis in Mice

被引:10
|
作者
Li, N. [1 ]
Zhang, L. [2 ]
Li, H. [3 ]
Fang, B. [1 ]
机构
[1] Zhengzhou Univ, Henan Tumor Hosp, Henan Inst Haematol, Henan Key Lab Expt Hematol, Zhengzhou 450008, Peoples R China
[2] Sun Yat Sen Univ, Ctr Canc, Dept Med Oncol, Guangzhou 510060, Guangdong, Peoples R China
[3] Zhengzhou Univ, Affiliated Hosp 1, Dept Pathol, Zhengzhou 450000, Peoples R China
关键词
BONE-MARROW-CELLS; HEMATOPOIETIC STEM-CELLS; NECROSIS-FACTOR-ALPHA; MYOCARDIAL-INFARCTION; LIVER FIBROSIS; CARBON-TETRACHLORIDE; INDUCED APOPTOSIS; IN-VIVO; REGENERATION; INFLAMMATION;
D O I
10.1016/j.transproceed.2010.09.010
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
On the basis of the recent report that granulocyte colony-stimulating factor (G-CSF) treatment significantly improves survival and liver histology among chemically injured mice, we investigated whether G-CSF administration could contribute to faster recovery and promote tissue repair after local liver irradiation. Bone marrow chimeric female C57BL/6 mice were treated with G-CSF at days 7, 14, and 21 after local liver irradiation. We assessed the fibrosis index and the origin of proliferating cells reconstituting the liver at 2 or 5 weeks after radiation challenge. At day 35 after local irradiation, we observed G-CSF treatment to significantly reduce radiation-induced liver damage and collagen deposition. In addition, hepatic hydroxyproline levels and serum fibrosis markers in mice receiving G-CSF administration after radiation challenge were significantly lower compared with those of control mice. More importantly, histological examination suggested that recovery from hepatic damage was much better among the G-CSF-treated mice. Immunofluorescence and fluorescence in situ hybridization analyses revealed that donor cells engrafted into the host liver displayed epithelium-like morphology and expressed albumin, albeit at low frequency. These results suggested that G-CSF treatment initiated endogenous hepatic tissue regeneration in response to radiation injury and ameliorated its fibrogenic effects.
引用
收藏
页码:3833 / 3839
页数:7
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