[Effects of ginkgolide B against damage of cultured hippocampal neurons caused by glutamate].

Aim: To investigate protective effects of ginkgolide B (GB) in different administration modes on glutamate-induced neuronal damage.

Methods: Essential GB were obtained by supercritical CO2 fluid extraction. Glutamate excitotoxicity were examined in primary cultures from neonatal Wistar rat, by using of Trypan blue dye staining, testing the lactate dehydrogenase leakage from cultured neurons and terminal deoxynucleotidyl transferase-mediated nick end labeling (TUNEL) method.

Neurogenesis in the adult rat brain after intermittent hypoxia.

Intermittent hypoxia has been found to prevent brain injury and to have a protective role in the CNS. To address the possible causes of this phenomenon, we made investigative effort to find out whether intermittent hypoxia affects neurogenesis in the adult rat brain by examining the newly divided cells in the subventricular zone (SVZ) and dentate gyrus (DG). The adult rats were treated with 3000 and 5000 m high altitude 4 h per day for 2 weeks consecutively.

Underlying mechanism of hypoxic preconditioning decreasing apoptosis induced by anoxia in cultured hippocampal neurons.

It is known that hypoxic preconditioning (HP, a brief period of sublethal hypoxia) provides neuroprotection against subsequent severe anoxia, but the mechanisms of this increased tolerance have not been fully elucidated. A hypoxic preconditioning model was established by exposing a 4-day hippocampal culture to 1% O(2) for 20 min/day for 8 days. The preconditioning significantly decreased the number of apoptotic neurons at reoxygenation 24 h after 4 h of severe anoxia (0% O(2)).

[Protective effect of Quinacrine on striatum neurons from heat treatment injury].

Aim: To study the protective effect of Quinacrine(QA) on rat striatum neurons from the injury caused by heat environment treatment, to probe the relationship between cell membrane injury and cellular injury protection, and to seek the possibility of QA as a preventive agent to heat injury.

Methods: Primary cultured striatum neurons from newborn rats were pretreated with QA at different concentration for 1 h, and then heat-treated at 43 degrees C for another 1 h. Cell necrosis was detected by Trypan blue staining, and apoptosis was evaluated through Activated Caspase-3 dye and TdT dye.

[Effects of hypoxia on the proliferation of embryonic stem cells].

Aim: To investigate the effects of hypoxia on the proliferation of mouse embryonic stem cells (mouse ES cells) in vitro.

Methods: We observed the proliferation of ES cells by hematometery and BrdU-labeled flow cytometry (FCM), and we also detected the expression of hypoxia inducible factor-1a (HIF-1a) by RT-PCR.

Results: (1) The number of ES cells after culturing in the hypoxia environment (3% O2 and 10% O2) for 24 hours were lesser than those in normoxia (20% O2).

Involvement of increased stability of mitochondrial membrane potential and overexpression of Bcl-2 in enhanced anoxic tolerance induced by hypoxic preconditioning in cultured hypothalamic neurons.

The effects of hypoxic preconditioning (HP) on changes in mitochondrial membrane potential (MMP) and Bcl-2 expression in cultured hypothalamic neurons after severe anoxia were investigated. In the HP group, hypothalamic neurons, after a 4-day culture, were preconditioned daily under a hypoxic condition (1% O(2), 10 min) for 8 days; subsequently, the HP neurons and those in the control group (similarly cultured, but without HP) were exposed to 6 h of severe anoxia (0% O(2)). The preconditioned neurons had a higher survival rate and a lower lactate dehydrogenase leakage, compared with the control group.

[Glutamate-neuroexcitotoxicity protective study of monoclonal antibody against human NMDA receptor key subunit].

Objective: To study if monoclonal antibody against human NMDA receptor key subunit (NR1) may protect neurons from excitotoxicity.

Methods: We cultured primary hippocampal neurons from 10 newborn rats and made the glutamate excitotoxicity model, examined the ratio of surviving neuron (Trypan blue dye staining) and LDH assay to study the protective effects of mAbN1, There were 2 plates in parallel per group, the experiments were repeated 4 times.

Results: 0.

[Effects of oxygen-glucose deprivation on cultured rat hippocampal neurons].

Aim: To investigate the effects of oxygen-glucose deprivation on cultured rat hippocampal neurons.

Methods: The hippocampal neurons cultured for 12 d were exposed to combined oxygen-glucose deprivation for 0.5 - 4 h and then cultured with original medium in normoxia for 28 h.

[Effects of naloxone on rat cortical neuron apoptosis induced by anoxia].

Objective: To investigate the damage of anoxia on the cultured rat's cortical neurons and the protective effects of naloxone.

Methods: Cortical neurons cultured for 12 days were randomly divided into three groups: control, anoxic group and anoxic group plus naloxone treated. Cortical neurons were exposed to anoxic environment for 6 hours and then cultured for 24 hours under normoxic condition.

[Effect of CoCl2 pretreatment on Na + and K+ currents of the rat hippocampal neurons after acute hypoxia].

Aim: To study effect of CoCl2 pretreatment on the voltage-gated Na+ and K+ currents of the rat hippocampal neurons after acute hypoxia.

Methods: Primarily cultured hippocampal neurons were divided into CoCl2 pretreated and non-pretreated groups. Patch clamp whole cell recording technique was used to examine Na+ and K+ currents of the hippocampal neurons.

[Establishment of the model of oxygen-glucose deprivation in vitro rat hippocampal neurons].

Aim: To establish the model of oxygen-glucose deprivation in vitro rat hippocampal neurons.

Methods: The hippocampal neurons cultured for 12 d were exposed to combined oxygen-glucose deprivation for 0.5-4 h and then cultured with original medium in normoxia for 24 h.

[CoCl2-induced enhancement of glucose transport activity in mediating hypoxic tolerance in cultured hippocampal neurons].

The effect of CoCl(2) pretreatment on glucose transport activity of cultured newborn rat hippocampal neurons and its role in neuronal hypoxic tolerance were observed. The results showed that the 2-deoxy-D-[1-(3)H ]glucose uptake rate and the mRNA expressions of glucose transporters (GLUT1 and GLUT3) in the hippocampal neurons were significantly increased after a 24-hour pretreatment with CoCl(2). The cell injury induced by 6-hour or 8-hour hypoxic exposure was also greatly reduced by CoCl(2) pretreatment.

[Effects of anoxia/reoxygenation on Fos and Jun expression and apoptosis in cultured rat hippocampal neurons].

Aim: To investigate the effects of anoxia/reoxygenation on Fos and Jun expression and apoptosis in cultured rat hippocampal neurons.

Methods: The hippocampal neurons cultured for 12 d were exposed to anoxia environment (90% N2 + 10% CO2) for 4 h and then reoxygenated for 24 h and 72 h. The neurons were immunocytochemically stained using the antiserum against Fos and Jun, and the apoptosis were detected by using the terminal deoxynucleotidyl transferase mediated biotinylated deoxyuridine triphosphate nickel end labeling (TUNEL) method and flow cytometric analysis.

[Effects of rhIL-6 on Bcl-2 and Bax expression and apoptosis after anoxia-reoxygenation in cultured rat hippocampal neurons].

The purpose of the present study was to determine the effects of recombinant human interleukin-6 (rhIL-6) on the Bcl-2 and Bax expression and apoptosis after anoxia-reoxygenation in cultured rat hippocampal neurons. The control and rhIL-6 treated hippocampal neurons cultured for 12 d were exposed to anoxia environment (90% N2+10% CO2) for 2 and 4 h and then were reoxygenated for 24 and 72 h. The expression of Bcl-2 and Bax was revealed immunocytochemically using the antiserum against Bcl-2 and Bax.

[Relationship between enhanced anoxic tolerance induced by hypoxic preconditioning and Na+, K+ currents in cultured hypothalamic cells].

Aim: To investigate the relationship between enhanced anoxic tolerance induced by hypoxic preconditioning and Na+, K+ currents.

Methods: After hypoxic preconditioning and acute anoxia the I(Na), I(K) were measured in cultured hypothalamic cells by patch-clamp whole cell recording technique.

Results: The amplification of Na+ currents did not been significantly changed, but the amplification of K+ currents was in hypoxic preconditioning neurons; acute anoxia lead to the inhibition of Na+, K+ currents in the two groups, while Na+, K+ currents in non-preconditioned control group were inhibited severity than hypoxic preconditioning group.

[Effects of hypoxic-preconditioning on anoxic-tolerance and Jun expression in cultured rat hippocampal neurons].

Aim: To study the effects of hypoxic preconditioning on anoxic tolerance and Jun expression in cultured rat hippocampal neurons after anoxia/reoxygenation.

Methods: 12 day cultured hippocampal neurons in control and hypoxic preconditioning group were exposed to anoxic environment (0.90L/L N2 + 0.