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Dendrobium nobile Lindl.alkaloids(DNLA),the active ingredients of a traditional Chinese medicine Dendrobium,have been shown to have anti-oxidative effects,anti-inflammatory action,and protective effect on neurons against oxygen-glucose deprivation.However,it is not clear whether DNLA reduces amyloid-beta(Aβ)-induced neuronal injury.In this study,cortical neurons were treated with DNLA at different concentrations(0.025,0.25,and 2.5 mg/L)for 24 hours,followed by administration of Aβ_(25–35)(10μM).Aβ_(25–35) treatments increased cell injury as determined by the leakage of lactate dehydrogenase,which was accompanied by chromatin condensation and mitochondrial tumefaction.The damage caused by Aβ_(25–35) on these cellular properties was markedly attenuated when cells were pretreated with DNLA.Treatment with Aβ_(25–35)down-regulated the expressions of postsynaptic density-95 mRNA and decreased the protein expression of synaptophysin and postsynaptic density-95,all changes were significantly reduced by pretreatment of cells with DNLA.These findings suggest that DNLA reduces the cytotoxicity induced by Aβ_(25–35) in rat primary cultured neurons.The protective mechanism that DNLA confers on the synaptic integrity of cultured neurons might be mediated,at least in part,through the upregulation of neurogenesis related proteins synaptophysin and postsynaptic density-95.
Dendrobium nobile Lindl.alkaloids (DNLA), the active ingredients of a traditional Chinese medicine Dendrobium, have been shown to have anti-oxidative effects, anti-inflammatory action, and protective effect on neurons against oxygen-glucose deprivation. However, it is not clear whether DNLA reduces amyloid-beta (Aβ) -induced neuronal injury. In this study, cortical neurons were treated with DNLA at different concentrations (0.025,0.25, and 2.5 mg / L) for 24 hours, followed by administration of Aβ_ (25 -35) (10 μM) .Aβ_ (25-35) treatments increased cell injury as determined by the leakage of lactate dehydrogenase, which was accompanied by chromatin condensation and mitochondrial tumefaction. The damage caused by Aβ_ (25-35) on these cellular properties was markedly attenuated when cells were pretreated with DNLA. treatment with Aβ_ (25-35) down-regulated the expressions of postsynaptic density-95 mRNA and decreased the protein expression of synaptophysin and postsynaptic density-95, all changes were s ignificantly reduced by pretreatment of cells with DNLA.These findings suggest that DNLA reduces the cytotoxicity induced by Aβ_ (25-35) in rat primary cultured neurons. The protective mechanism that DNLA confers on the synaptic integrity of cultured neurons might be mediated, at least in part, through the upregulation of neurogenesis related proteins synaptophysin and postsynaptic density-95.