Evidence map›Paper›PMID 29435803›Full record

ArticleNeurochemical research2018

Rifampicin Prevents SH-SY5Y Cells from Rotenone-Induced Apoptosis via the PI3K/Akt/GSK-3β/CREB Signaling Pathway.

Xia Wu, Yanran Liang, Xiuna Jing, Danyu Lin, Ying Chen, Tianen Zhou, Sudan Peng, Dezhi Zheng, Zhifen Zeng, Ming Lei and 2 more

Abstract read
PubMed Publisher
In one paragraph

Article in Neurochemical research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
3.7field-weighted citation impact, top 7% 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

30 citing papers in PubMed, 53 citations in OpenAlex.

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  8. Roles of THEM4 in the Akt pathway: a double-edged sword.Journal of Zhejiang University. Science. B · 2024
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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

12 authors at 1 institution in 1 country.

Xia WuDepartment of Neurology, The Sun Yat-sen Memorial Hospital of Sun Yat-sen University, No. 107 Yanjiang West Road, Guangzhou, 510080, Guangdong, China.
Yanran LiangDepartment of Neurology, The Sun Yat-sen Memorial Hospital of Sun Yat-sen University, No. 107 Yanjiang West Road, Guangzhou, 510080, Guangdong, China.
Xiuna JingDepartment of Neurology, The Sun Yat-sen Memorial Hospital of Sun Yat-sen University, No. 107 Yanjiang West Road, Guangzhou, 510080, Guangdong, China.
Danyu LinDepartment of Neurology, The Sun Yat-sen Memorial Hospital of Sun Yat-sen University, No. 107 Yanjiang West Road, Guangzhou, 510080, Guangdong, China.
Ying ChenDepartment of Neurology, The Sun Yat-sen Memorial Hospital of Sun Yat-sen University, No. 107 Yanjiang West Road, Guangzhou, 510080, Guangdong, China.
Tianen ZhouDepartment of Emergency, The Sun Yat-sen Memorial Hospital of Sun Yat-sen University, No. 107 Yanjiang West Road, Guangzhou, 510080, China.
Sudan PengDepartment of Neurology, The Sun Yat-sen Memorial Hospital of Sun Yat-sen University, No. 107 Yanjiang West Road, Guangzhou, 510080, Guangdong, China.
Dezhi ZhengDepartment of Neurology, The Sun Yat-sen Memorial Hospital of Sun Yat-sen University, No. 107 Yanjiang West Road, Guangzhou, 510080, Guangdong, China.
Zhifen ZengDepartment of Neurology, The Sun Yat-sen Memorial Hospital of Sun Yat-sen University, No. 107 Yanjiang West Road, Guangzhou, 510080, Guangdong, China.
Ming LeiDepartment of Neurology, The Sun Yat-sen Memorial Hospital of Sun Yat-sen University, No. 107 Yanjiang West Road, Guangzhou, 510080, Guangdong, China.
Kaixun HuangDepartment of Neurology, The Sun Yat-sen Memorial Hospital of Sun Yat-sen University, No. 107 Yanjiang West Road, Guangzhou, 510080, Guangdong, China.
Enxiang TaoDepartment of Neurology, The Sun Yat-sen Memorial Hospital of Sun Yat-sen University, No. 107 Yanjiang West Road, Guangzhou, 510080, Guangdong, China. taoenxiang@163.com.ORCID http://orcid.org/0000-0001-8493-4983
Sun Yat-sen University · CN

Funding

Fundamental Research Fund for University Youth Scholars 17ykpy39Guangzhou Science and Technology Research Project 201607010219National Natural Science Foundation of China 81371391National Natural Science Foundation of China 81503052National Natural Science Foundation of China 81571244National Natural Science Foundation of China 81771378Natural Science Foundation of Guangdong Province 2014A030313202Natural Science Foundation of Guangdong Province 2016A030313322Natural Science Foundation of Guangdong Province 2017A030313840Public Welfare Research and Capacity Building Project of Guangdong Province 2014A020212164
6 · The paper itself

Abstract

In addition to its original application for treating tuberculosis, rifampicin has multiple potential neuroprotective effects in chronic neurodegenerative diseases including Parkinson's disease (PD) and Alzheimer's disease. Inflammatory reactions and the PI3K/Akt pathway are strongly implicated in dopaminergic neuronal death in PD. This study aims to investigate whether rifampicin protects rotenone-lesioned SH-SY5Y cells via regulating PI3K/Akt/GSK-3β/CREB pathway. Rotenone-treated SH-SY5Y cells were used as the cell model to investigate the neuroprotective effects of rifampicin. Cell viability and apoptosis of SH-SY5Y cells were determined by CCK-8 assay and flow cytometry, respectively. The expression of Akt, p-Akt, GSK-3β, p-GSK-3β, CREB and p-CREB were measured by Western blot. Our results showed that the cell viability and level of phospho-CREB significantly decreased in SH-SY5Y cells exposed to rotenone when compared to the control group. Both the cell viability and the expression of phospho-CREB in cells pretreated with rifampicin were higher than those of cells exposed to rotenone alone. Moreover, pretreatment of SH-SY5Y cells with rifampicin enhanced phosphorylation of Akt and suppressed activity of GSK-3β. The addition of LY294002, a PI3K inhibitor, could suppress phosphorylation of Akt and CREB and activate GSK-3β, resulting in abolishment of neuroprotective effects of rifampicin on cells exposed to rotenone. Rifampicin provides neuroprotection against dopaminergic degeneration, partially via the PI3K/Akt/GSK-3β/CREB signaling pathway. These findings suggest that rifampicin could be an effective and promising neuroprotective candidate for treating PD.

Indexed as

ApoptosisCell Line, TumorCell SurvivalCyclic AMP Response Element-Binding ProteinEnzyme InhibitorsGlycogen Synthase Kinase 3 betaHumansPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsProto-Oncogene Proteins c-aktRifampinRotenoneSignal TransductionCREB1 protein, humanCyclic AMP Response Element-Binding ProteinEnzyme InhibitorsGlycogen Synthase Kinase 3 betaPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsProto-Oncogene Proteins c-aktRifampinRotenonecAMP response element-binding proteinGlycogen synthase kinase-3βNeuroprotectionRifampicinRotenone

Identifiers

PMID29435803
OpenAlexW2793177201

What OpenQuestion holds

Textmetadata
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Registered trials

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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 OpenQuestion graph.