| Objective: Angiogenesis depends on the interaction of a variety of promoting factorsand inhibiting factors. Notch signaling pathway take part in this process. Deferasirox is anew iron chelator, can induce the secretion of hypoxia-inducible factor HIF, finally, affectthe expression of VEGF. This experiment investigates the effect of deferasirox on narrowpedicle and random flap Dll4and CD105expression and angiogenesis in rats.Methods:20SD rats were randomly divided into the deferagirox group and thecontrol group (n=10). Rats were subjected to deferagirox of100mg. kg-1.d-1in theexperimental groups respectively and same dose saline in the control group for1week. Ineach group, flap were created and made in each rats’bilateral back. ratio of length to widthof tissue in the pedicle portion and the flap portion respectively was:1cm×1cm,3cm×3cm.The tissue samples were taken from the pedicle and the flap portions of the flap. The Dll4and CD105expression was also detected with immunohistochemistry method (SABC).Results: Compared with control group, whatever in the pedicle portion or the flapportion, there was a significantly increase of flap microvessels marked by CD105(P<0.05)and a significantly decrease of flap microvessels stained by Dll4(P<0.05) in thedeferagirox group. In both two groups, Compared with the pedicle portion, there was asignificantly increase of flap microvessels marked by CD105and Dll4in the the flapportion (P<0.05).Conclusions: deferasirox can increase the CD105expression and angiogenesis ofslender narrow pedicle random flap.This process might be related to the inhibition of Dll4 protein expression, which was significant in the notch signaling pathway. |