Deferoxamine inhibits microglial activation, attenuates blood–brain barrier disruption, rescues dendritic damage and improves spatial memory in a mouse model of microhemorrhages
Journal of Neurochemistry
Xiao-fei He1,†, Yue Lan2,†, Qun Zhang3, Dong-xu Liu3, Qinmei Wang4, Feng-ying Liang1, Jin-sheng Zeng1, Guang-qing Xu3,* andZhong Pei1,*
DOI: 10.1111/jnc.13657

Abstract
Cerebral microbleeds are strongly linked to cognitive dysfunction in the elderly. Iron accumulation plays an important role in the pathogenesis of intracranial hemorrhage (ICH). Deferoxamine (DFX), a metal chelator, removes iron overload and protects
against brain damage in ICH. In the present study, the protective effects of DFX against microhemorrhage were examined in mice. C57BL6 and Thy-1 GFP transgenic mice were subjected to perforating artery microhemorrhages on the right posterior parietal
cortex using two-photon laser irradiation. DFX (100 mg/kg) was administered 6 h after microhemorrhage induction, followed by every 12 h for three consecutive days. The water maze task was conducted 7 days after induction of microhemorrhages, followed by
measurement of blood-brain barrier permeability, iron deposition, microglial activation, and dendritic damage. Laser-induced multiple microbleeds in the right parietal cortex clearly led to spatial memory disruption, iron deposits, microglial activation
and dendritic damage, which were significantly attenuated by DFX, supporting the targeting of iron overload as a therapeutic option and the significant potential of DFX in microhemorrhage treatment.

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