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Article Publish Status: FREE
Abstract Title:

Neuroprotective effects of genistein on SH-SY5Y cells overexpressing A53T mutantα-synuclein.

Abstract Source:

Neural Regen Res. 2018 Aug ;13(8):1375-1383. PMID: 30106049

Abstract Author(s):

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

Article Affiliation:

Huan-Cheng Wu

Abstract:

Genistein, a potent antioxidant compound, protects dopaminergic neurons in a mouse model of Parkinson's disease. However, the mechanism underlying this action remains unknown. This study investigated human SH-SY5Y cells overexpressing the A53T mutant ofα-synuclein. Four groups of cells were assayed: a control group (without any treatment), a genistein group (incubated with 20 μM genistein), a rotenone group (treated with 50 μM rotenone), and a rotenone + genistein group (incubated with 20 μM genistein and then treated with 50 μM rotenone). Alactate 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 1 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-SY5Y cells. Compared with the control group, the expression of NFE2L2 and HMOX1 was significantly increased in the genistein + rotenone group. However, after treatmentwith 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 disease. Genistein can reduce oxidative stress damage and cell apoptosis by activating estrogen receptors and NFE2L2 channels.

Study Type : Animal Study, In Vitro Study

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Sayer Ji
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