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Objective To establish an early cognitive disorder model in rats and investigate the early cognitive functioning after ischemic hypoxic brain injury during the neonatal period. Methods Forty-six newborn Sprague-Dawley rats were randomized into a 21-d-old group and a 31-d-old group. These 2 groups were then subdivided into model and sham-operated subgroups (M21, n=12; SH21, n=11; M31, n=12; SH31, n=11). A model of neonatal early cognitive disorder was established in the rats of the M21 and M31 groups using a modification of Rice's method. Rats in the SH21 and SH31 groups received skin incisions and common carotid artery separation without ligation or hypoxia. Each group was tested with a Morris water maze. The rats were sacrificed after testing, and brain tissue was examined under the electron microscope. Nissl staining allowed Nissl body quantification and neurocyte acin the M21 group was significantly longer than in the SH21 group. The 31-d-old subgroups had shorter average escaping latencies than the corresponding 21-d-old subgroups. (b) Spatial memory: The average platform times, Ⅰ region times and Ⅰ region distances showed no significant differences among groups. ②Brain pathology (a) Gross appearance: Obvious ischemic hemisphere atrophy was observed in the M group, and no abnormality was observed in the SH group. (b) Electron microscopic observation: In the SH group cell ultrastructures in the ischemic hippocampus were normal. Karyopyknosis and dilated endoplasmic reticulums were found in the M group. More mitochondria were found in the presynaptic membranes of the ischemic hippocampus in the M group than that in the SH group. (c) Nissl body quantification and neurocyte activity analysis: Significantly less activity in the ischemic cortex was found in the M21 group compared to the SH21 group. More activity was observed in the 31-d-old subgroups than in the corresponding 21-d-old subgroups. Conclusions ①The neonatal rats with ischemic hypoxic brain injury had prolonged average escaping latency and depressed neuronal activity. ②The 31-d-old rats had better spatial localization learning ability than the 21-d-old rats.
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Objective To observe the effect of apigenin on the recovery of neurological function following cerebral ischemia-reperfusion and investigate its mechanism. Methods Ninety male Sprague-Dawley rats were randomized into a sham-operated group, a model group and an apigenin-treated group. A transient ( 1.5 h) focal cerebral ischemia-reperfu-sion model was established in the rats of the model and apigenin-treated groups. In the sham-operated rats the middle cere-bral artery was not occluded. The rats in the apigenin-treated group received an intra-abdominal injection of apigenin, and the rats in the other two groups received injections of normal saline solution. Neurological behavior scores were assessed in accordance with the Zea Longa method at the 24th, 48th and 72nd hour and the 7th day after reperfusion. Cellular and sub-cellular morphology were observed with an optical microscope and an electron microscope, and the levels of TNF-α and IL-1β were measured using ELISA. Results Neurological function improved by the 7th day after reperfusion in the model group, but improved significantly by the 72nd hour after reperfusion in the apigenin-treated group. Average TNF-α and IL-1β levels in the model group and the apigenin-treated group were significantly higher than in the sham-operated group. Av-erage TNF-α and IL-1β levels in the apigenin-treated group were significantly lower than in the model group at the 48th and 72nd hour after reperfusion. Neurological behavior scores had a positive correlation with the IL-1β and TNF-α levels. In the model group, obvious intracellular and intercellular edema and vacuolization were observed in the ischemic cortices and hippocampuses, with remarkable karyopycnosis and organelle broadening and dissolution and vacuolization in glial cells and neurons. In the apigenin-treated group, similar but significantly milder morphological changes were observed. Conclusion Apigenin can promote the recovery of neurological function in rats by downregulating the expression of TNF-α and IL-1βfollowing focal cerebral ischemia-reperfusion.
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@#Objective To study the characteristic findings on magnetic resonance imaging (MRI) in children with cerebral palsy (CP) induced by chronic kernicterus.Methods The MR imagings in 13 CP cases induced by chronic kernicterus were retrospectively studied, which were compared with 6 healthy and age-matched controls. 13 cases were finally diagnosed as dyskinetic cerebral palsy (athetoid subtype).Results In 13 cases, all showed symmetric high signals in the the globus pallidus on T2-weighted imaging. There were not apparent abnormality on T1-weighted imaging.Conclusion The bilateral high intensity signals in the globus pallidus on T2-weighted imaging are the characteristic findings on MRI in CP children induced by chronic kernicterus. Paying attention to the globus pallidus on MRI may be useful in determining the type of cerebral palsy.
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Objective To study the inhibition of iron-dependent lipid peroxidation(IDLPO)by apigenin on rat cerebral homogenate in vitro and to evaluate the neuroprotective effects of apigenin on acute transient focal cerebral ischemia-reperfusion injury in rats.Methods In vitro IDLPO on rat cerebral homogenate was induced with ferrous sulfate,the incubation mixture was observed at three various concentration of apigenin and deferoxamine(DFX),and malondialdehyde(MDA)level was assayed by the 2-thiobarbituric acid(TBA)test.In vivo,the transient focal cerebral ischemia-reperfusion model in rats was established with insertion of thread embolish into middle cerebral artery.In experiment groups the neurological behavior scores,TTC stain of brain slices,and neurocyte morphology were observed.The homogenate of left hemisphere was collected for investigating the effect of apigenin on content of MDA and activity of superoxide dismutase(SOD)in 24,48,and 72 h.Results MDA was reduced in three various concentration of apigenin on rat cerebral homogenate(P0.05).In vivo,abnormal neurological behavior scores existed and typical cortical infarct lesions were found by TTC stain in both apigenin and model groups.An obvious intracellular and intercellular edema and vacuolization were found in the cerebral cortexes and hippocampuses in model group.There was karyopycnosis in glias and neurons.However lesion was alleviated in apigenin group.The MDA contents in both apigenin and model groups were increased greatly compared to ones of Sham-operated group,respectively(P