The effects of deferoxamine on inhibition for microglia activation and protection of secondary nerve injury after intracerebral hemorrhage in rats.

To investigate the effects of the iron chelatordeferoxamine (DFA) on inhibition formicroglia activation and protection of secondary nerve injury after intracerebral hemorrhage (ICH) in rats. The rats were randomly divided into sham operation group, ICH group and DFA treatment group. The collagenase was used to prepare ICH model of basal gangliain rats and 1h after the beginning of the operation, the intraperitoneal injection with DFA was arranged every 12 h and for a total of 7d. The changes of Iron ion concentration were measured at perihematomaat different time points after the medicine was given. OX42 immunohistochemical staining observed microglia change at perihematoma. ELISA method determined the changes of IL-1β and TNF-β content of brain tissue. Neurological deficit scores and Nissl staining were used to observe the situation of neurological function and neuronal loss of rats after DFA treatment. 1 d After the start of ICH, the concentration of iron in perihematoma was significantly higher than that of animalsin sham-operated group and could sustain for28 d. At the same time, the quantities of local microglial cells were significantly increased. After applying DFA, the concentration of iron ions in the brain tissue around the hematoma was significantly reduced, so did the number of microglial cells and activation of neurotoxic cytokines (IL-1β and TNF-α content) secreted by microglial cells was significantly reduced. At the same time, the loss of neurons in the tissue around of the hematoma was significantly reduced and neurological deficit scores were significantly reduced. Iron ions which were sustainedly released by hematoma after ICH can activate the local microglia and cause secondary brain injury. DFA curb excessive activation of microglia and reduce neuronal death of ICH by means of clearinf away iron ions of brain tissue surrounding the hematoma, thus improve secondary neurological dysfunction.