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OBJECTIVE To investigate the effect of quercetin on primary cultured newborn rat cortex neuron cell which is estrogen depletion, and discuss the possible mechanism, to provide new ideas and strategies for developing a drug of neurodegenerative disease. METHODS Rat cortex neurons were isolated from one day old Sprague Dawley rats and treated with estrogen, quercetin and estrogen receptor antagonists (ICI182,780). Cell viability was determined by MTT assay, neurite outgrowth was measured by fluorescent microsope and estrogen receptors were determine by Western blot. RESULTS Quercetin functions like estrogen to increase cortex neuronal cell viability, the Que (50, 100 μmol·L-1) group compared with the control group could significantly improve the activity of the cortical neurons(P<0.05). It can also increase neurite out growth, the Que (50,100 μmol·L-1) group significantly promoted the formation of synapse, most of the neurons were full, and the synapses of neurons became thick, growth, and connect to a dense neural network. And in the Western blot experiments, Que (50, 100 μmol·L-1) group could obviously increase the expression of estrogen receptor alpha protein, in addition, the neural protective effect of quercetin can be inhibited by ICI182,780. CONCLUSION Quercetin like estrogen can protected cortex neuronal and the effect of quercetin on cortex neuronal cells was mediated by estrogen receptor alpha.
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OBJECTIVE:The effects of zinc fructose diphosphate(ZnFDP)in different concentrations on the growth of cultured newborn mouse cerebral cortex neurons were observed METHODS:The newborn mice cerebral cortex neurons were cultured and different dosages of ZnFDP were added with final concentrations of 2 5?g/ml,12 5?g/ml and 125?g/ml The convert phase microscope was used to observe the growth of dendrites and cell bodies of neurons The survival neuron count and LDH assay were carried out to investigate the effect of ZnFDP on the growth and development of neurons in different culture periods RESULTS:After 48h,the number and the length of neural dendrites in 12 5?g/ml ZnFDP group were increased but the maximum diameter of cell bodies of neurons showed no change There were no significant differences in all parameters observed between 2 5?g/ml group and control group,while 125?g/ml ZnFDP obviously inhibited the differentiation of neurons The survival neurons on 12 5?g/ml ZnFDP group outnumbered those in the control group after 3d,7d and 10d culture,and the LDH activity in 12 5?g/ml ZnFDP group was lower than that in control group after 7d and 10d culture CONCLUSION:This study suggests that a suitable dose of ZnFDP can promote the growth and development of cerebral cortex neurons
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Aim To investigate protective effects and mechanism of TPG on ischemia_like injury models. Methods Six ischemia models including hypoxia, hypoglucose, oxidant injury, calcium overload, nitric oxide neurotoxicity and excitatory amino acid injury were used to assay the anti_ischemic roles of TPG in cultured primary cortex neurons. Results It was found that TPG possessed obvious protective effects on primary neurons in injury models by the way of morphological examination. Crystal violet staining also indicated that TPG increased number of life neurons in injury models significantly. Couclusions 50～200 ?g?ml-1 TPG protected rat cortex cells from all injury models effectively in vitro.
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Objective: To investigate the effects and mechanism of transhinone on calcium overloaded injuried models.Methods: Three injured models induced by caffeine, KCI, and NMDA, respectively, were used to assay the action of tanshinone in cultured primary cortex neurone of baby rats. Results: It was found that tanshinone possessed obvious protective effects on primary neurone in injured models by the way of morphological examination. Crystal violet staining and lactic dehydrogenase (LDH) measurement in supernate also indicated that tanshinone increased number of live neurone and reduced the extent of cell injury significantly.Conclusion: Tanshinone protected rat cortex cells from three kinds of calcium overloadied injured effectively in vitro.
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Objective To study whether neuronal injury induced by platelet activating factor (PAF) was involved in NMDA /PSD 93 signaling pathway.Methods Primary cortex neurons culture were from wild type and PSD 93 knockout mice.Then the neurons were pretreated with 0.3 ?mol/L PAF for 24 hours, 5 ?mol/L BN52021, 10 ?mol/L MK-801, or 60 ?mol/L L-NAMA, respectively. The cells were stained with PI/Calcein for apoptosis detection. Varied protein expressions were also observed in the neurons by western blot. Proteins colocalized on neuraxon were detected by cell immunochemistry and confocol microscopy, and cGMP activity was measured by radioimmunoassay.Results (1) PSD 95, NR2A, and nNos except PSD 93 expressed in the cortex neurons from PSD 93 knockout mice. (2) PSD 93, NR2A and nNos colocalized on neurite. (3) Neurotoxicity and cGMP avtivity induced by PAF decreased in PSD 93 knockout cortex neurons.Conclusion NMDA/PSD 93 signaling pathway is involved in neuronal injury induced by PAF.
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AIM To investigate protective effects and mechanism of tanshinones on ischemia-like injury models. METHODS Six ischemia models including hypoxia, hypoglucose, oxidant injury, caffeine injury, nitric oxide neurotoxicity and excitatory amino acid injury were used to assay the anti-ischemic roles of tanshinones in cultured primary cortex neurons. The changes of injuried cortex neurons were observed by the way of morphological examination, and live neurons of crystal violet staining were measured according to absorbent index. RESULTS it was found that tanshinones possessed obvious protective effects on primary neurons in injury models by the way of morphological e~nation. Crystal violet staining also indicated that tanshinones increased number of live neurons in injury models significantly. The protective effects of tanshinones on models of oxidant injury, caffeine injury and NMDA injury were superior to other injury models. CONCLUSIONS 83.0 ?mol? L- 1 tanshinones protected rat cortex cells fm all injury models effectively in vitro.