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Neuroprotective effects of genistein on sh-SY5Y cells overexpressing A53T mutant α-synuclein

Neural Regeneration Research 2018年第8期13卷 1375-1383页

作者： Huan-Cheng Wu Qun-Liang Hu shi-Jun Zhang Yan-Min Wang Zhan-Kui Jin Ling-Fu Lv Sai Zhang Zhen-Lin Liu Hong-Lian Wu Ou-Mei Cheng Graduate School Tianjin Medical University Tianjin China Tianjin Beichen Hospital Tianjin China Tianjin Key Laboratory of Neurotrauma Repair Institute of Traumatic Brain Injury and Neuroscience Center for Neurology and Neurosurgery of Affiliated Hospital Logistics University of Chinese People's Armed Police Force Tianjin China Department of Clinical Medicine Chongqing Medical University Chongqing China

Genistein, a potent antioxidant compound, protects dopaminergic neurons in a mouse model of Parkinson＇s disease. However, the mecha- nism underlying this action remains unknown. This study investigated human sh-sysy cells overexpressing the A53T mutant of α-synuclein. Four groups of cells were assayed： a control group （without any treatment）, a genistein group （incubated with 20 μM genistein）, a rote- none group （treated with 50 μM rotenone）, and a rotenone ＋ genistein group （incubated with 20 μM genistein and then treated with 50μM rotenone）. A lactate dehydrogenase release test confirmed the protective effect of genistein, and genistein remarkably reversed mitochondrial oxidative injury caused by rotenone. Western blot assays showed that BCL-2 and Beclin ! levels were markedly higher in the genistein group than in the rotenone group. Terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling revealed that genistein inhibited rotenone-induced apoptosis in sh-sysy cells. Compared with the control group, the expression of NFE2L2 and HMOX1 was significantly increased in the genistein ＋ rotenone group. However, after treatment with estrogen receptor and NFE2L2 channel blockers （ICI-182780 and ML385, respectively）, genistein could not elevate NFE2L2 and HMOX1 expression. ICI-182780 effectively prevented genistein-mediated phosphorylation of NFE2L2 and remarkably suppressed phosphorylation of AKT, a protein downstream of the estrogen receptor. These findings confirm that genistein has neuroprotective effects in a cell model of Parkinson＇s dis- ease. Genistein can reduce oxidative stress damage and cell apoptosis by activating estrogen receptors and NFE2L2 channels.

关键词： nerve regeneration genistein neuroprotection sh-sysy cells Parkinson＇s disease rotenone estrogen receptor NFE2L2 A53T a-synuclein oxidative stress neurodegeneration neural regeneration

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