Biological Activity |
Deferoxamine mesylate is an iron chelator, and effectively reduces oxidative stress and neuronal death. In Vitro: Deferoxamine treatment significantly increases HIF-1alpha binding under all culture conditions, including hypoxic and high-glucose. The mechanism of deferoxamine is through improving HIF-1alpha biological function through scavenging oxygen free radicals[1]. Deferoxamine (5 uM) has significant effect on the tumor-associated stromal cells cellular multiplication, and cells die at day 7 after exposure to 50 uM and 100 uM deferoxamine. Deferoxamine (5 uM-100 uM) inhibits the proliferation of BMMSCs, and induces apoptosis of MSCs in a dose-dependent manner. Deferoxamine influences the expression of adhesion proteins on MSCs[3]. Deferoxamine (30, 60, 120?uM) shows lower expression of HIF-1alpha in a concentration dependent way in AdMSCs[4]. In Vivo: Deferoxamine (100 mg/kg, i.p.) lowers the mortality rate of subarachnoid hemorrhage (SAH) rat. Deferoxamine (100 mg/kg, i.p.) attenuates Evan�s blue extravasation in cortex, ameliorates the tight junction detachment and preserves the integrity of the base membrane examined in electron microscope at day 3 after SAH. Deferoxamine attenuates degradation of BBB proteins after SAH and significantly reduces ferritin expression at day 3 in the cortex, and improves neurologic behavior and cognitive deficits after experimental[1]. Ten uL of 1 mM deferoxamine-treated wounds display significantly accelerated healing from day 7 onward and heal significantly faster than control-treated wounds in diabetic mice. Deferoxamine-treated wounds and dimethyloxalylglycine-treated wounds heal significantly faster than control-treated wounds in aged mice[2]. In deferoxamine (10 mg/mL)-treated TG mice, there is a decrease in both soluble and insoluble Abeta40 and Abeta42. Both pGSK3beta and beta-catenin are significantly increased by approximately 50% in the deferoxamine-treated mice[5]. |