Home > Browse Issues > Vol.36 No.2
Neuroprotective Effect of Selenomethionine Against Injury Induced by Aβ1-42 in N2a Cells
Wen Lei1, Chen Chen1, Shi Qingxue1, Zhang Zhonghao1, Ying Ming1, Song Guoli1*, Yang Silin2, Song Yun2
1College of Life Sciences, Shenzhen University, Shenzhen 518060, China; 2Huaxin Bio-pharmaceutical Co. Ltd., Jieshou 236500, China
Abstract: To investigate the effect of Selenomethionine (Se-Met) on amyloid beta peptide (Aβ)1-42-induced neurotoxicity in Neuro-2A (N2a) cells， N2a cells were divided into 4 subgroups: control， Aβ1-42 model， Se-Met-treated and Se-Met-preincubated Aβ1-42 model group. Cell viability was evaluated by CCK-8 kit and the result showed that different concentrations of Se-Met had different effect on N2a cell viability. Aβ1-42 treatment significantly decreased cell viability compared to the control group， while Se-Met preincubation attenuated Aβ1-42-induced cell viability loss (P<0.05). Levels of ROS (reactive oxygen species) were measured by DCFH-DA probe kit. Pretreatment with Se-Met significantly decreased the level of ROS in Aβ1-42 treated cells (P<0.05). Meanwhile， Se-Met pretreatment significantly restored the levels of synaptophysin and PSD95 and inhibited Aβ1-42-induced increase in the level of LC3-II/LC3-I (P<0.05). These data suggested that Se-Met could increase N2a cell viability at a certain concentration and a period of time， inhibit the increase of ROS generation and autophagy， and ameliorate the synaptic loss induced by Aβ1-42. Thus， Se-Met plays an important role in neuroprotection of Aβ-induced neuronal toxicity.
CN
EN