Evidence map›Paper›PMID 27229883›Full record

ArticleNeurotoxicity research2016

β-Ecdysterone Protects SH-SY5Y Cells Against 6-Hydroxydopamine-Induced Apoptosis via Mitochondria-Dependent Mechanism: Involvement of p38(MAPK)-p53 Signaling Pathway.

Zhi Pan, Yingcai Niu, Yini Liang, Xiaojie Zhang, Miaoxian Dong

Abstract read
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In one paragraph

Article in Neurotoxicity research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

11 citing papers in PubMed, 19 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

5 authors at 2 institutions in 1 country.

Zhi PanCenter for New Medicine Research, Changchun University of Chinese Medicine, Changchun, 130117, China.
Yingcai NiuThe Institute of Medicine, Qiqihar Medical University, 333 BuKui Street, Jianhua District, Qiqihar, 161006, China.
Yini LiangThe Institute of Medicine, Qiqihar Medical University, 333 BuKui Street, Jianhua District, Qiqihar, 161006, China.
Xiaojie ZhangThe Institute of Medicine, Qiqihar Medical University, 333 BuKui Street, Jianhua District, Qiqihar, 161006, China.
Miaoxian DongThe Institute of Medicine, Qiqihar Medical University, 333 BuKui Street, Jianhua District, Qiqihar, 161006, China. dmx1969@126.com.
Qiqihar Medical University · CNChangchun University of Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Parkinson's disease (PD) is a neurological disorder pathologically characterized by loss of dopaminergic neurons in the substantia nigra. No curative therapy is available for PD. We recently found that phytoestrogen β-ecdysterone (β-Ecd) is able to reduce MPP(+)-induced apoptosis in PC12 cells. This study investigated the potential of β-Ecd to protect against SH-SY5Y cell apoptosis induced by the PD-related neurotoxin 6-hydroxydopamine (6-OHDA) and the underlying mechanism for this cytoprotection. In the present study, pretreatment with β-Ecd significantly reduced 6-OHDA-induced apoptosis of SH-SY5Y cells by a mitochondria-dependent pathway, as indicated by downregulation of Bax and PUMA (p53 upregulated modulator of apoptosis) expression, suppressing ΔΨm loss, inhibiting cytochrome c release, and attenuating caspase-9 activation. Furthermore, we showed that the inhibition of p38 mitogen-activated protein kinase (p38(MAPK))-dependent p53 promoter activity contributed to the protection of SH-SY5Y cells from apoptosis, which was validated by the use of SB203580 or p38β dominant negative (DN) mutants. Additionally, knock-down apoptosis signal-regulating kinase 1 (ASK1) by specific shRNA and blockade reactive oxygen species (ROS) by pharmacological inhibitor competently prevented β-Ecd-mediated inhibition of p38(MAPK) and ASK1 phosphorylation, respectively. These data provide the first evidence that β-Ecd protects SH-SY5Y cells against 6-OHDA-induced apoptosis, possibly through mitochondria protection and p53 modulation via ROS-dependent ASK1-p38(MAPK) pathways. The neuroprotective effects of β-Ecd make it a promising candidate as a therapeutic agent for PD.

Indexed as

Antiparkinson AgentsApoptosisApoptosis Regulatory Proteinsbcl-2-Associated X ProteinCaspase 9Cell Line, TumorCell SurvivalCytochromes cDrug Evaluation, PreclinicalEcdysteroneHumansMAP Kinase Kinase Kinase 5MAP Kinase Signaling SystemMitochondriaOxidopaminep38 Mitogen-Activated Protein KinasesAntiparkinson AgentsApoptosis Regulatory ProteinsBAX protein, humanBBC3 protein, humanbcl-2-Associated X ProteinCASP9 protein, humanCaspase 9Cytochromes cEcdysteroneMAP3K5 protein, humanMAP Kinase Kinase Kinase 5Oxidopaminep38 Mitogen-Activated Protein KinasesProto-Oncogene ProteinsReactive Oxygen SpeciesTumor Suppressor Protein p53ApoptosisMitochondrial membrane potentialp38MAPKParkinson’s diseaseβ-Ecdysterone

Identifiers

PMID27229883
OpenAlexW2405993884

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.