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AIM: To observe the neuroprotective effect of combined treatment with taurine and diazepam against focal cerebral ischemia-reperfusion in rats. METHODS: Sixty male Sprague-Dawley rats were randomly divided into five groups: sham-operation group, vehicle group, taurine group (200 mg/kg, ip), diazepam group (10 mg/kg, ip) and combined treatment group (taurine 100 mg/kg+diazepam 5 mg/kg). Focal cerebral ischemia was induced by the method of middle cerebral artery occlusion (MCAO) in rats, and reperfusion was emerged by removing the thread 2 h later. The drugs were administered respectively at the time of reperfusion, and subsequently repeated once 12 h later. The animals in vehicle group were intraperitoneally injected with isodose normal saline. The neurological deficit score, the brain water content and cerebral infarction were measured 48 h after MCAO. Other 5 group animals of focal cerebral ischemia-reperfusion (n=16 in each group) were set up as mentioned above and accepted treatments 10 h after reperfusion, likewise repeated once 12 h later. Twelve animals in each group were adopted the same management as the previous 5 groups at 48 h after MCAO. The remained 4 animals in each group were sacrificed until two weeks after MCAO to observe the histopathological changes by nissl staining. RESULTS: Compared to vehicle group, the animals in combined treatment group at 2 h or 12 h after MCAO both decreased the neurological deficit score, reduced the brain water content and infarct volume (P<0.01 or P<0.05). The combined treatment significantly alleviated the neurological necrosis as well. The neuroprotective effect of the combined treatment was superior to that of using taurine or diazepam alone. CONCLUSION: These results suggest that combination of taurine and diazepam treatment has a coordinate neuroprotective effect on both the acute and chronic brain damage of focal cerebral ischemia-reperfusion.
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Objective To study the effects of γ-aminobutyric acid (GABA) and sertraline on the cognition functions in acute stressed rats.Methods Y-type maze were used to test the cognitive function of Male SD (Sprague-Dawley) rats.They were exposed to the forced-swimming stress test,which was to make acute stress model of depression.Except control group,rats were pretreated with different doses of GABA and/or sertraline,then the time of immobility in the forced-swimming test and latency in the maze were observed individual.Results Compared with the model group[(1404.33±129.46)s] ,GABA could decrease the immobility time obviously in the forced-swimming test [(432.33±187.64) s ＞ (332.50±217.23) s,P ＜ 0.01].Otherwise the immobility time was prolonged with 0.50 g/kg GABA + 10 mg/kg sertraline (1086.17±411.80) s (P ＜ 0.05).Compared with the control group(105.00±32.18)s,the latency in the maze was prolonged remarkably in the model group (179.17±8.54) s(P＜ 0.05).Pretreatment with 10 mg/kg sertraline(100.30±21.01) s or GABA and sertraline groups (69.83±16.89) s,(86.83±13.11) s (P ＜ 0.05 or 0.01) could decrease the latency.Conclusion GABA could play its role of antagonizing acute depression.Meanwhile,pretreatment with appropriate doses of GABA and sertraline not ordy could decrease doses of two drugs but also improve the cognitive function in the acute stress rats.
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Objective To investigate the feature and general trend of the contingent negative variation (CNV) in the aged with memory impairment (AMI) and dementia tendency in the course towards advanced dementia. Methods CNV in 69 AMI subjects (serving as the study group) and 22 healthy elderly subjects selected from well age matched (serving as the control group) were examined. Hasegawa's dementia scale for the aged (HDS) in all AMI were also examined. 2 3 years later, 22 from the study group were examined again. The wave forms and relevant indexes of CNV were observed and analyzed. Results Reaction time(RT)〔(284.3?170.6) ms vs (149.8?101.7) ms, P
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Middle cerebral artery occlusion(MCAO) can be used to establish the standard model of focal cerebral ischemia.The method for establishing focal cerebral ischemia model has been improved continuously,from simple behavior score,measurement of infarcted brain area,and morphological observation in the past to functional study,neurobiochemistry,molecular biology,etc.The research of MCAO provides a basis for further study of the pathological characteristics,mechanism and prevention of human cerebral ischemia.This article reviews the recent advancement in the study of MCAO model and cerebral(ischemia.)
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Objective To study the effects of the monomers of ginsenoside Rb1 (GSRb1) on the concentrations of intracellular calcium in ischemic neurons of rats.Methods Hippocampus neurons from embryo of rats were cultured in vitro, then placed into normal extracellular fluid (normal control group), simulated ischemic extracellular fluid (ischemia group), simulated ischemic extracellular fluid without calcium (ischemia without calcium group) and simulated ischemic extracellular fluid with different concentration of GSRb1. The fluorescence intensity of intracellular calcium in each group was measured by laser scanning confocal microscope technique, and the corresponding percentage was calculated by comparison with normal control.Results Compared with normal control group, fluorescence intensity of intracellular calcium increased by ( 73.5?10.31)% in ischemia group, ( 4.5?2.58)% in ischemia without calcium group,( 20.2?3.41)%, ( 13.6?2.98)%,( 10.5?3.62)% and ( 12.7?4.51)%, respectively, in simulated ischemic extracellular fluid with different concentration of GSRb1 groups (20, 40, 60 and 80 ?mol/L). The decreases of fluorescence intensity of intracellular calcium in simulated ischemic extracellular fluid with different concentration of GSRb1 groups were significantly different compared with ischemia group (all P
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Objective To observe the influence of ginsenoside Rb3(GSRb3) on ?-aminobutyric acid (GABA) in brain tissue of rats with injury of hypoxia.Methods 20 rats were randomly divided into A, B, C, D and E group. The models of cerebral anoxia in group A and C were made by hypopiesia and hypoxia, and the models of hypoxia-reoxgenation were made in group B and D. 24 h and 1 h before establishment of models, ginsenoside Rb3 was injected peritoneally in rats of group C and D, respectively. The number and form of GABA-like immunoreactive neurons in hippocampus CA1 area of rats after brain hypoxia-reoxgenation were investigated with immunohistochemistry.Results (1)Compared with group E, GABA-like immunoreactive neuron density in CA1 area of group A and B decreased, presented with light staining and absence of prominency. GABA-like immunoreactive neuron density in CA1 area in group C and D was significantly higher than that in group A and B, but the shape was similar to group E. (2) The number of GABA-like immunoreactive neuron in CA1 area was 7.7?2.83 (group A), 10.1?2.08 (group B), 30.9?2.02 (group C), 33.1?4.2 (group D) and 16.9?1.05 (group E), respectively. The numbers were lower in group A and B than in group E, however higher in group C and D than in group E(all P
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Objective To study the protective effect of Acathopanax Senticosus(AS) to the neuron by toxicity of Glu.Methods With hippocampal slice in rats and histography technique,we observed the effect in OPS of ischemic hippocampal slice by Glu between AS group and no AS group,and the changes of ultrastructure in the two groups were also observed.Results In AS group OPS was decreased and disappeared after slice with Glu for 5 min,the recovery rate of OPS was 16.6%,the degree was 41.5%.There was significant difference in the two groups( P