Background: Edaravone (Eda) is a free-radical scavenger which is used in treating stroke, cerebral hemorrhage and some other diseases in clinic. However, it’s antioxygenation during development is still unknown.
Method: An oxidative damage model was established in chick embryo by using a generator of free radicals, 2,2’-azobis[2-methylpropionamidine] dihydrochloride (AAPH). The mortality rate and embryo’s weight were measured to detect whether retarded growth happened. In order to observe the blood vessels, the yolk-sac blood vessels and CAM blood vessels density were observed. The malondialdehyde (MDA) content and superoxide dismutase (SOD) enzymatic activity were detected to evaluate the oxidative damage in the chick embryo.
Result: In this model, embryo development and angiogenesis were heavily affected by AAPH. However, Eda alleviated the growth retardation and anti-angiogenesis induced by AAPH. After AAPH treatment, the MDA content increased and SOD enzymatic activity declined which was also mitigated by Eda.
Conclusion: Overall, our research revealed that Eda mitigated embryonic anti-angiogenesis induced by oxidative damage after AAPH treatment, which may be helpful for future clinical studies.
Published on: Dec 1, 2016 Pages: 19-22