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Brain cell microenvironment,also known as cerebral tissue channel,consists of the brain extracellular space and its contents.For a long time,because of the limit of technology,the research about brain extracellular space hasn't been given enough attention in the field of cognitive sciences and neuroscience.With the development of medical imaging technology,the research about brain extracellular space will open up a new space for brain and cognitive sciences,and provide a new approach for diagnosis and treatment of encephalopathy.Based on the method of medical informatics,this article reveals hot topics on brain science,presents the history of the research about brain cell microenvironment,and analyzes the construction of neurology literature so as to provide reference for the future researchers.
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Aim To study the action mechanism of hyperin(Hyp) on neonatal rat's neuron with anoxia/reoxygenation(A/R).Methods The dissociated neonatal rat brain cells were subjected to 30 min of anoxia or followed 40 min of reoxygenation.Lactate dehydrogenase(LDH),malondialdehyde(MDA)and nitric oxide(NO)in the supernatant were measured.The intracellular free calcium concentration([Ca~(2+)]_i)in brain cells was assayed with Fura 2-AM method.Results Anoxia induced a significant increase of LDH in the supernatant from (62.0±13.0) U·L~(-1)(Sham group)to (116.0±16.6) U·L~(-1)(Control group,P<0.01),and reoxygenation markedly increased LDH and MDA in the supernatant from (45.6±9.2) U·L~(-1) and (9.1±0.9) μmol·L~(-1)(Sham group)to (106.0±17.4) U·L~(-1) and (16.4±2.7) μmol·L~(-1)(Control group,P<0.01),respectively.In the range of 1.0 ～ 16.0 μmol·L~(-1),Hyp markedly and concentration-dependently inhibited anoxia-or reoxygenation-evoked increases of LDH and MDA.1.0～16.0 μmol·L~(-1) Hyp not only inhibited anoxia-induced increase of NO in the supernatant and rise of [Ca~(2+)]_i in brain cells(P<0.05 or P<0.01),but also attenuated reoxygenation-evoked increases of NO and[Ca~(2+)]_i(P<0.05 or P<0.01),Hyp 16.0 μmol·L~(-1) significantly reduced NO and[Ca~(2+)]_i from (34.4±6.3) μmol·L~(-1) and (640±94) nmol·L~(-1) to (25.0±5.1) μmol·L~(-1) and (331±56) nmol·L~(-1),respectively.Conclusion The protective effect of Hyp on A/R-injured neurons may be related to the inhibition of overload of[Ca~(2+)]_i,NO release and lipid peroxidation.
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Objective To explore theDNA damage of brain cells of goldfishs through formaldehyde exposure.Methods The goldfishs were treated with liquid formaldehyde at different concentrations(0.01 mmol/L,0.1 mmol/L和1mmol/L)for three days.Single cell gelelectrophoresis technique(comet assay)was used to test the DNA damage of the brain cells.Results Formaldehyde caused significant DNA strand break at the concentration of 0.01mmol/L,0.1mmol/L and 1.0mmol/L.Conclusions Formaldehyde was both a DNA strand breaker when the concentration is higher,it may cause crosslinkagent to the brain in vivo.
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Objective To observe the effect of Cyclosporine A on the brain immunoligical reject reaction of transgenic cellular transplant in rats with experimental brain hemorrhage.Methods We established the brain hemorrhagic models of rats and the models were divided into group A (treated with Cyclosporin A) and group B (without treatment) randomly after transplanting brain cells modified by NGF gene. The levels of CD~+_4, CD~+_8T cells subsets in peripheral blood were examined by using flow cytometry at 15 d after transplantation. The expressions of MHC-classⅡantigens and infiltration of CD~+_4, CD~+_8T lymphocyte subsets were examined by SP immunocytochemical stain.Results The count of CD~+_4, CD~+_8T lymphocyte and CD~+_4/CD~+_8 in peripheral blood were 29.20?3.97, 20.65?2.02 and 1.41?0.86 in group A, and were 47.39?3.01, 28.30? 2.36 and 1.68?0.69 in group B, respectively.There were significant differences between the two groups (all P