Protective effects of astaxanthin on Aβ_(25~35)-induced damage in cultured mouse cortical neurons
LU Ya
Abstract
LU Ya
Abstract
Objective To investigate the neuroprotective effects of astaxanthin(AST) on Aβ25~35 induced damage in cultured mouse cortical neurons.Methods Cultured cortical neurons were incubated with AST for 2 h and then were exposed to 10 μmol/L aged Aβ25~35 for 24 h.The cell viability was evaluated by MTT assay,cell apoptosis was observed by Hoechst 33342 staining,the changes of intracellular reactive oxygen species levels and mitochondrial membrane potential were measured by DCFH-DA and Rhodamine 123 probes,respectively.Results AST,over a concentration range of 500 ~ 4 000 nmol/L,attenuated 10 μmol/L Aβ25~35-induced cell viability loss and decreased the reactive oxygen species levels.2 000 nmol/L AST pretreatment significantly restored the mitochondrial membrane potential and inhibited Aβ25~35-induced apoptosis.Conclusions Pretreatment with AST exhibits noticeable neuroprotection against cortical neuron damage induced by Aβ25~35 and the protective effects of AST on mitochondria functions maybe partly responsible for it.
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Objective To investigate the neuroprotective effects of astaxanthin(AST) on Aβ25~35 induced damage in cultured mouse cortical neurons.Methods Cultured cortical neurons were incubated with AST for 2 h and then were exposed to 10 μmol/L aged Aβ25~35 for 24 h.The cell viability was evaluated by MTT assay,cell apoptosis was observed by Hoechst 33342 staining,the changes of intracellular reactive oxygen species levels and mitochondrial membrane potential were measured by DCFH-DA and Rhodamine 123 probes,respectively.Results AST,over a concentration range of 500 ~ 4 000 nmol/L,attenuated 10 μmol/L Aβ25~35-induced cell viability loss and decreased the reactive oxygen species levels.2 000 nmol/L AST pretreatment significantly restored the mitochondrial membrane potential and inhibited Aβ25~35-induced apoptosis.Conclusions Pretreatment with AST exhibits noticeable neuroprotection against cortical neuron damage induced by Aβ25~35 and the protective effects of AST on mitochondria functions maybe partly responsible for it.
Key concepts: Neuroprotection, Viability assay, Reactive oxygen species, Apoptosis, Rhodamine 123, Cortical neurons, Intracellular, Molecular biology