Effects of ginkgo biloba extract on the cognitive function and expression profile of inflammatory factors in a rat model of hemorrhagic stroke.

Hemorrhagic stroke is a major risk factor for cognitive impairment. Our study aimed to measure the effect of ginkgo biloba extract (EGB761) on the cognitive ability and inflammatory expression in hemorrhagic stroke model SD rats and to analyze their relationship. Forty SD rats were divided randomly into an SD group (normal control SD rats), an SD+EGB761 group (normal control SD rats supplemented with 45 mg/kg EGB761), a CO group (hemorrhagic stroke model SD rats using collagenase), and a CO+EGB761 group (hemorrhagic stroke model SD rats supplemented with 45 mg/kg EGB761) consisting of 10 rats, respectively. The Y-electric maze test was selected to measure the cognitive function in four groups. Furthermore, enzyme-linked immunosorbent assay and real-time PCR were, respectively, applied for detecting the protein and gene expression profiles of inflammatory factors in primary cultured microglia. Compared with rats in the SD group, the average time of electrical simulation for mastering criteria was prolonged in the CO group (P<0.05). Furthermore, expression levels of proinflammatory cytokines interleukin-1ß (IL-1ß), IL-6, and tumor necrosis factor-α and anti-inflammatory cytokines IL-4, IL-10, and tumor necrosis factor-ß were significantly increased and decreased, respectively, in rats of the CO group compared with the SD group (P<0.05). The results of electrical simulation time, inflammatory factors protein, and gene expression profile in rats of the CO+EGB761 group compared with the CO group were opposite to above contrast (P<0.05). Ginkgo biloba extract could alleviate the cognitive dysfunction after hemorrhagic stroke in SD rats; this is associated with regulating the expression of inflammatory factors secreted by microglia.

Reduced cerebral blood flow in genetic prion disease with PRNP D178N-129M mutation: an arterial spin labeling MRI study.

The D178N mutation in the PRNP gene is associated with fatal familial insomnia and Creutzfeldt-Jakob disease (CJD). Typically, the D178N mutation associated with the 129M genotype is related to fatal familial insomnia while the same mutation associated with the 129V genotype is linked to familial CJD. We describe a D178N-129M haplotype in a patient with early, severe dementia and late-onset minor insomnia, mainly presenting as the CJD phenotype. Cerebrospinal fluid 14-3-3 protein was positive. Diffusion weighted imaging demonstrated widespread cortical ribbon-like high signal intensity, which was also seen in the basal ganglia bilaterally. Arterial spin labeling (ASL) MRI showed severe hypoperfusion in the cerebral cortex, basal ganglia and thalami but this was least marked in the thalami. Neuroimaging abnormalities were more prominent in the cerebral cortex than the thalamus, which was in line with the clinical picture of severe dementia rather than insomnia. ASL-MRI seems to be a useful tool for the detection and follow-up of perfusion changes in patients and asymptomatic carriers harboring the PRNP mutation.

[Influence of hyperbaric oxygen treatment on neural plasticity in experimental rats].

OBJECTIVE: To explore the influence of hyperbaric oxygen (HBO) treatment on neural plasticity and it's mechanism in experimental rats with cerebral ischemia. METHODS: Ninety-healthy male adult Sprague-Dawley rats (3 to approximately 4 month old) were randomly divided into a pseudo-operative group, a model group, and an HBO therapy group. The middle cerebral artery occlusion model was duplicated with suture methods, then we used beam walking test (BWT) to determine the motor skill of the rats and immunohistochemistry method to detect the distribution and location of microtubule-associated protein-2 (MAP-2) and glial fibrillary acidic protein (GFAP). Quantitative real-time PCR was used to detect the expression of Map-2 mRNA and GFAP mRNA. RESULTS: Immunohistochemistry showed that the fluorescence gray scale value of Map-2 in the HBO group was the highest in 3 groups at 1st week and 2nd week (P<0.05).The value of GFAP was lower than that of the model group but higher than that of the sham operated group (P<0.05). Real-time fluorescence-quantitative PCR indicated that the Map-2 mRNA of HBO group was the highest in 3 groups at 1st week and 2nd week (P<0.05); but the value of GFAP mRNA in the HBO group is lower than that of the model group,but higher than that of the sham operated group at 1st week and 2nd week (P<0.05). CONCLUSION: After cerebral infarction, giving hyperbaric oxygenation treatment can improve the limbs motor function, and hyperbaric oxygenation treatment can increase the expression of Map-2 and decrease the expression of GFAP, which promote neural plasticity.