虾青素对Aβ_(25～35)诱导小鼠皮层神经元损伤的保护作用

Protective effects of astaxanthin on Aβ_(25～35)-induced damage in cultured mouse cortical neurons

目的研究虾青素(AST)对Aβ25～35诱导小鼠皮层神经元损伤的保护作用。方法原代培养的小鼠皮层神经元用AST预孵育2 h,再与老化的10μmol/L Aβ25～35共孵育24 h。采用MTT法测定细胞活力,Hoechst 33342染色观察细胞凋亡,DCFH-DA荧光法检测细胞内ROS水平,Rhodamine 123荧光法检测线粒体膜电位。结果 500～4 000 nmol/L的AST预处理能有效抑制10μmol/L Aβ25～35诱导的神经元活力下降,降低细胞内ROS的水平。2 000 nmol/L AST对神经元线粒体膜电位的保护作用最明显,能显著抑制神经元凋亡。结论 AST对Aβ25～35诱导小鼠皮层神经元损伤有明显的保护作用,其机制可能和保护线粒体功能有关。

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.