Abstract
Introduction The hematopoietic growth factor erythropoietin (EPO) plays an important role in apoptosis and oxidative stress attenuation as well as the promotion of angiogenesis in several tissues. Systemically administered EPO has beneficial effects on rabbits subjected to subarachnoid hemorrhage or stroke. So far, the angiogenic effect of EPO has been documented after an experimentally induced stroke or subarachnoid hemorrhage. In our study, we examined the possible angiogenic effect of chronic treatment with recombinant human erythropoietin (rHuEPO) under normal conditions, in an attempt to clarify if the existence of a lesion or oxygen deprivation is necessary to initiate the angiogenic effect of EPO. Materials & methods BALB/c mice were used and were divided into three groups as follows: group A (no treatment), group B (saline only), and group C (7000 U rHuEPO per week for three weeks by intraperitoneal injection). The number of CD31- and CD34-positive endothelial cells was assessed in mouse brain preparations under control conditions and after treatment with rHuEPO. Results There was no difference between the mean numbers of CD31 and CD34 cells among the different groups. The mean number of vessels in group A and group B was almost the same (18 ± 2 vessels per optical field). However, the number of brain vessels in group C (EPO treatment) increased significantly by 44% compared to controls (26 ± 4 vessels per optical field, P < 0.05). Conclusion These data indicate that no lesion or oxygen deprivation is needed to initiate the angiogenic effect of EPO in healthy mouse brains.