Evidence map›Paper›PMID 30106049›Full record

ArticleNeural regeneration research2018

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

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

Open access · goldAbstract read
In one paragraph

Article in Neural regeneration research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 2 pooled it
1.9field-weighted citation impact, top 14% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

23 citing papers in PubMed, 2 syntheses or guidelines pooled it, 52 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 3 institutions in 1 country.

Huan-Cheng WuGraduate School, Tianjin Medical University; Tianjin Beichen Hospital, Tianjin, China.
Qun-Liang HuTianjin Beichen Hospital, Tianjin, China.
Shi-Jun ZhangTianjin Beichen Hospital, Tianjin, China.
Yan-Min WangTianjin Beichen Hospital, Tianjin, China.
Zhan-Kui JinTianjin Beichen Hospital, Tianjin, China.
Ling-Fu LvTianjin Beichen Hospital, Tianjin, China.
Sai ZhangTianjin 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.
Zhen-Lin LiuTianjin 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.
Hong-Lian WuDepartment of Clinical Medicine, Chongqing Medical University, Chongqing, China.
Ou-Mei ChengDepartment of Clinical Medicine, Chongqing Medical University, Chongqing, China.
Tianjin Beichen Hospital · CNChinese People's Armed Police ForceChongqing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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 of α-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). 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 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 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 disease. Genistein can reduce oxidative stress damage and cell apoptosis by activating estrogen receptors and NFE2L2 channels.

Indexed as

A53Testrogen receptorgenisteinnerve regenerationneural regenerationneurodegenerationneuroprotectionNFE2L2oxidative stressParkinson's diseaserotenoneSH-SY5Y cellsα-synuclein

Identifiers

PMID30106049
PMCPMC6108222
OpenAlexW2887364005

What Socratic holds

Textmetadata
LicenceCC BY-NC-SA
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.