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Objective To explore the effect of erythropoietin (EPO) on cognition and neuron apoptosis in CA1 region of hippocampus in vascular dementia (VaD) rats.Methods 54 Wistar rats were randomly divided into three groups:sham control group,VaD group,VaD+ EPO group (n=18,each).The bilateral common carotid arteries of Wistar rats were permanently ligated to establish VaD models.Spatial study and memory were observed by Y maze test at 4,8 and 12 weeks after operation.Neuron apoptosis in CA1 area of hippocampus was measured by terminal deoxynucleotidyl-transferase (TdT) mediated dUTP-biotin nick end labeling (TUNEL) method.The protein and mRNA expressions of Bcl 2 and Bax in CA1 region of hippocampus were detected by immunohistochemistry and RT-PCR at 4,8,12 weeks after operation.Results Compared with VaD group,the VaD+ EPO group had better performances including less error reaction times and shorter total reaction time in Y-maze (both P＜0.05) at 4,8,12 weeks after operation.The apoptotic neuronal cells in CA1 region of hippocampus was decreased in VaD+ EPO group than in VaD group at 4,8,12 weeks after operation [(10.50±±2.43) vs.(20.50±± 3.29),(23.92±±3.18) vs.(33.58±3.48) and (36.92±4.10) vs.(54.17±4.26),t=4.23,3.54,5.05,P=0.013,0.024,0.007,respectively].The Bcl-2-positive cells and Bcl-2 mRNA expression were increased,and the Baxpositive cells and Bax mRNA expression were decreased in VaD+ EPO group than in VaD group (all P ＜0.05).Conclusions Erythropoietin can improve cognitive function by inhibiting neuron apoptosis through regulation of Bcl-2 and Bax expression in CA1 region of hippocampus.
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Objective:To study the role of adhesion molecules in the pathogenesis of polymyositis. Methods:The abnormal expression of adhesion molecules on T cells in peripheral blood and muscle fibers from patients with myositis was analyzed by two colour immunofluoresence and RT PCR methods respectively. Results:The expression of adhesion molecules including lymphocyte function associated antigen 1(LFA 1 ),very late antigen 4(VLA 4) on T cells in peripheral blood and intercellular adhesion molecule l(ICAM 1) on muscle fibers from patients with myositis was markedly higher than that in the healthy control group. Conclusion: These findings suggested that adhesion molecules may be responsible for the migration of T cells and destraction of muscle fibers.
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Objective To study the expression of prepro-orexin mRNA in circadian rhythms and sleep-deprived rats.Methods Sleep was deprived with “rotation cylinder” in rats. RT-PCR was used to determine the change of prepro-orexin mRNA expression in cortex and hypothalamus of circadian rhythms and sleep-deprived rats.Results There was a significant changes of prepro-orexin mRNA expression with circadian rhythms in hypothalamus of rats. But there was no significant change in cortex. More prepro-orexin mRNA expression was found in hypothalamus than in cortex of rats. The expression of prepro-orexin mRNA in hypothalamus and in cortex of rats was not effected by short times of sleep deprivation. However the expression was raised by a 8-hour sleep deprivation.Conclusions There should be a close relationship between orexin and sleep. The control of sleep may be dependent on regulation of orexin in hypothalamus.
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AIM: To investigate the effect of antisense oligodeoxynucleotides (AS-ODN) on the intercellsular adhesion molecule-1(ICAM-1) expression on endothelial cells in hypoxia/reoxygenation(H/R). METHODS: With cultured glomerular vascular endothelial cell in H/R,the positive percentage of ICAM-1 expression was measured by flow cytometry before and after giving AS-ODN. RESULTS: The ICAM-1 expression did not increase on glomerular vascular endothelial cell in 10 hours hypoxia compared to control group,it increased in 6 hours reoxygenation, and decreased by 40.6% after giving AS-OND. CONCLUSION: AS-ODN may decrease the expression of ICAM-1 on endothelial cells in H/R.
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AIM: To investigate the effect of antisense oligodeoxynucleotides (AS - ODN) on the intercellsular adhesion molecule- 1 (ICAM- 1 ) expression on endothelial cells in hypoxia/reoxygenation(H/R). METHODS: With cultured glomerular vascular endothelial cell in H/R, the positive percentage of ICAM - 1 expression was measured by flow cytometry before and after giving AS - ODN. RESULTS: The ICAM - 1 expression did not increase on glomerular vascular endothelial cell in 10 hours hypoxia compared to control group, it increased in 6 hours reoxygenation, and decreased by 40.6 % after giving AS- OND. CONCLUSION: AS - ODN may decrease the expression of ICAM- 1 on endothelial cells in H/R.
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Objective:To observe the expression changes of adhesion molecules in peripheral blood leukocytes and serum soluble adhesion molecules in acute ischemic stroke after treatment with bartroxobin. Methods:Treatment group( n =8) was given bartroxobin (20 BU in 3 d) and other routine treatment;Control group( n =18) was similar to treatment group except for bartroxobin.The expression of CD11b,CD18,CD62L,CD54 on polymorphonuclear and monocyte were measured by flow cytometry, soluble ICAM 1 and VCAM 1 were measured by enzyme linked immunosorbent assay in consecutive patients[within 12,24,48 h( P
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Objective: To study caspase-3 activities and the neuroprotective effect of caspase-3 inhibitor Ac-DEVD-CMK in primary cultures of rat hippocampal neurons during hypoxia/reoxygenation (H/R). Methods: After pretreated with Ac-DEVD-CMK or the vector DMSO fo 1 h, primary cultures of rat hippocampal neurons were induced to hypoxia for 3 h, followed by 12 to 48 h of reoxygenation. The neuronal viability was estimated by MTT assay, and caspase-3 cellular activities were measured by a colorimetric method using Ac-DEVD-pNA as a substrate. Results: During H/R, the cultured rat hippocampal neuronal viability gradually decreased, and caspase-3 activities in the primary cultures of rat hippocampal neurons were significantly increased, and peaked at 24 h of reoxygenation. Caspase-3 activities were decreased in the neurons pretreated with Ac-DEVD-CMK in a dose dependent manner. Conclusion: Delayed neuronal death is detected in cultured hippocampal neurons during H/R, and apoptosis mediated by caspase-3 may play an important role in it, and caspase-3 inhibitor has a neuroprotective effect on them.
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Objective To evaluate the efficacy and safety in treatment of patients with mild to moderate Alzheimer’s disease (AD). Methods A total of 233 patients with mild to moderate potential AD were enrolled in a 16-week multi-center double blind clinical trial. All patients were randomized into two groups. 110 patients in galantamine group and 108 patients in donepezil group were enrolled in efficacy analysis. The scales of Alzheimer’s Disease Assessment Scale-Cognitive Subscale (ADAS-cog), Alzheimer’s Disease Cooperative Study Activities of Daily Living Scale (ADCS-ADL) and The Neuropsychiatric Inventory (NPI) were used to assess the effect at both baseline and the end of 16 weeks. Safety issues, including vital signs, lab assays and ECG examinations were measured. Results Patients in both groups were obviously improved in the total score of ADAS-cog (-5.4?6.4) in the galantamine group and (-4.0?7.3) in the donepezil group, P=0.098). 76% patients of the galantamine group had a score of ADAS-cog less than 20 at the end of 16 weeks treatment, which was higher than that of the donepezil group (58%, P=0.015). The sub-score of speech ability in ADAS-cog were improved in the galantamine group (baseline 2.8?2.9,16 weeks 1.8?2.5) compared with the donepezil group (baseline 2.8?3.0, 16 weeks 2.3?2.9, P=0.035). No significant difference of ADSC-ADL and NPI scale was found between the two groups (P=0.447 and 0.936 respectively). The sleep/night behavior was improved in the donepezil group (baseline 14%, 16 weeks 10%) compared with the galantamine group (baseline 23%, 16 weeks 22%, P=0.012). Two drug-related severe adverse events occurred during the trial, which were platelet reduction in the galantamine group and acute drug-induced hepatic injury in the donepezil group. The incidence of adverse events was 44% in the galantamine group and 47% in the donepezil group respectively. Galantamine had little influence on vital signs and lab assays. Conclusion Safe and well tolerated, galantamine improves the cognition, activities of daily living and neuropsychiatric symptoms of patients with mild to moderate AD.
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Objective To study the role of caspase 3 in ischemic brain damage of rats, and further understand the molecular mechanisms of ischemic cerebral vascular disease.Methods Rat models of the left middle cerebral artery (MCA) occlusion/reperfusion were made using a modification of the intraluminal sature method of Longa established by Belayev, infarct zones were confirmed by 2,3,5 triphenyltetrazolium chloride (TTC) staining, and caspase 3 expression on brain sections at the mRNA and active protein level was detected with in situ hybridization and immunohistochemistry technique, respectively.Results After 2 hours of left MCA ischemia followed by 24 hours of reperfusion, obvious infarct in the MCA dominate regions was confirmed by TTC staining; low levels of caspase 3 mRNA, and fewer of its active protein expression was found in normal brains, sham brains and contralateral brains of MCAO rats; both caspase 3 mRNA and activated protein expression in ipsilateral region were increased after 24 hours of recirculation, and even higher levels were detected at 48 hours of reperfusion.Conclusion Apoptotic mechanism might involve in delayed neuronal death after cerebral ischemia, and caspase 3 might play an important role in ischemic neuronal injury.
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2.0 g/L,the ratio of CSF and blood glucose ratio
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Apurinic/apyrimidinic endonuclease/redox factor 1(APE/Ref 1) is a multifunctional protein that is responsible for repairing DNA damage,it also infleunce reduction oxidation (redox) reaction and modulate the DNA binding activity of transcription factors,it is important to cell survival.Recently, much data concerning APE1/Ref 1 and information on APE1/Ref 1 in a wide variety of functions and systems have rapid growth,including its gene,function,distribution and relations with some diseases,especially nervous system diseases and tumors.