Abstract: Background Granulocyte colony-stimulating factor（G-CSF）has been reported to have beneficial effect on cardiac dysfunction in post infarction and doxorubicin-induced cardiomyopathy.Objective To investigate the effects of G-CSF on cardiac remodeling in cardiac hypertrophy induced by angiotensin Ⅱ（Ang Ⅱ）.Methods Thirty-six male wild type mice（WT）were allocated randomly to receive subcutaneously G-CSF（10 μg/kg per day, n=9）,or Ang Ⅱ（2.88 mg/kg per day,n=9）,or Ang Ⅱ plus G-CSF（Ang Ⅱ 2.88 mg/kg+G-CSF 10 μg/kg,n =9）for 4 weeks with untreated WT（n=9）as controls.Blood pressure and cardiac function were measured. Heart weight/body weight ratio,myocyte cross-sectional area and fibrosis area were determined.The mRNA ex- pression of osteopontin（OPN）in myocardium was detected by RT-PCR.The expressions of angiotensin converting enzyme（ACE）,ACE2 and phosph-p70S6 kinase protein in myocardium were assessed by Western-Blot.Results Ang Ⅱ significantly elevated blood pressure（SBP,Ang Ⅱ:139.7±1.6 vs WT:108.7±2.3 mmHg,P＜0.05） and caused cardiac hypertrophy and fibrosis.G-CSF treatment did not prevent the Ang Ⅱ-induced elevation of blood pressure（SBP,Ang Ⅱ+G-CSF:140.1±2.6 vs Ang Ⅱ:139.7±1.6 mmHg,P＞0.05）,but significantly attenuated the myocyte cross-sectional area（Ang Ⅱ+G-CSF:181.06±0.11 vs Ang Ⅱ:202.02±0.16 μm~2,P＜ 0.05）,fibrosis area（Ang Ⅱ+G-CSF:2.87%±0.12% vs Ang Ⅱ:3.91%±0.06%,P＜0.05）,heart weight/ body weight ratio（Ang Ⅱ+G-CSF;3.7±0.2 vs Ang Ⅱ:4.2±0.1 mg/g,P＜0.05）,and left ventricular diastolic function（cardiac isovolumic relaxation time,Ang Ⅱ+G-CSF:0.11±0.02 vs Ang Ⅱ:0.16±0.01 ms,P＜0.05）. Further more,G-CSF reduced cardiac levels of ACE,OPN,phosph-p70S6 kinase and increased the expression of ACE2.Conclusion These data suggest that G-CSF reduces Ang Ⅱ induced hypertrophy.The effect of G-CSF on the prevention of cardiac fibrosis and hypertrophy was associated with the inhibition of OPN and phosph-p70S6 ki- nase expression.