We assessed neurological outcomes, infarct volume, and the expression of nestin and caspase-3 in the hippocampal dentate gyrus following middle cerebral artery occlusion (MCAO) followed by reperfusion, with mild hypothermia (MH) treatment at the onset of ischemia in a MCAO rat model. Reperfusion began 2 hours after the MCAO model was set-up. MH treatment began at the onset of ischemia and was maintained for 4 hours. We evaluated neurological deficit score, brain infarct volumes, along with the immunohistochemical staining of nestin and caspase-3 in the sub-granular zone of the injured hemisphere on the 1st, 3rd, 7th, and 14th day after the onset of ischemia. Correlations between the number of nestin-positive (nestin+) cells, caspase-3-positive (caspase-3+) cells with infarct volume, as well as neurological deficit scores, were evaluated by linear regression. MH significantly promoted survival, reduced mortality, improved neurological deficit score, reduced brain infarct volume, increased the number of neural stem/progenitor cells and inhibited neuronal apoptosis in the sub-granular zone of the injured hemisphere. The number of nestin+ cells correlated with neurological deficit score in the normothermic group, and with infarct volume in the hypothermia group except for the first day after the onset of ischemia. The number of caspase-3+ cells correlated with the neurological deficit score but not infarct volume. The neuroprotective effects of MH may be mediated by modulating neural stem/progenitor cells and neuronal apoptotic cells in the sub-granular zone of the injured hemisphere during cerebral ischemia/reperfusion injury.
Objective To investigate the expression of HIF-1α in the brain tissue around the hemorrhagic foci in intracerebral hemorrhage(ICH) and its correlation with the time of ICH and brain edema.Methods 56 SD rats were randomly divided into pseudooperation group,and groups of 6,24,72 h;7,14,and 21 d after ICH.There were 8 rats for each group.The model of ICH was established in rats by intracerebral injection of autogenous blood.The expressions of HIF-1α in brain tissue around the hemorrhagic foci and the normal brain tissue were detected with SP immunohistochemical method.The expression of HIF-1α was compared with the degree of brain edema at different time points after ICH.Results The positive expression rates of HIF-1α were 60.4%(29/48) in ICH brain tissue and 0% in normal brain tissue,and the difference was significant(P0.01).The expression was gradually enhanced with the increase of time after ICH(P0.01).The expression reached a peak level at 72 h and persisted for 7 days and then declined gradually.After ICH,the level of cerebral water content raised gradually and peaked at 72 h(P0.01).There was a positive correlation between the level of water content and HIF-1α expression(P0.01).Conclusion HIF-1α is over expressed in the brain tissue around the hemorrhagic foci of ICH,and there is a positive correlation between the level of water content and HIF-1α expression.
Objective To investigate the effect of hyperbaric oxygen on HIF-1α expression and brain edema in rats with intracerebral hemorrhage. Methods Eighty-eight SD rats were randomly divided into sham group, ICH group and HBO group. Then ICH group and HBO group were divided into 6 h, 24 h, 3 d, 7 d and 14 d subgroups. Immunohistochemistry was applied to detect the levels of HIF-1α. The water content in rat brains was detected to determine the effects of HBO on the expression of HIF-1α in brain after intracerebral hemorrhage. Results Compared with sham group, the water content in ICH group and HBO group were significantly increased (P0.05), and the levels of HIF-1α were also significantly increased (P0.05). There were statistically significant difference in the levels of HIF-1α between ICH group and HBO group on the 14th day after intracerebral hemorrhage (P0.05). There were a positive correlation between the levels of water content and HIF-1α labeling index in ICH group (P0.05), while a negative correlation in HBO group (P0.05). Conclusion The expression of HIF-1α may be involved in the formation of brain edema after ICH. HBO retreatment may inhibit the expression of HIF-1α and reduce the formation of brain edema.
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