Evidence map›Paper›PMID 25257523›Full record

ArticleInternational journal of molecular sciences2014

Inhibition of autophagy via activation of PI3K/Akt pathway contributes to the protection of ginsenoside Rb1 against neuronal death caused by ischemic insults.

Tianfei Luo, Guiying Liu, Hongxi Ma, Bin Lu, Haiyang Xu, Yujing Wang, Jiang Wu, Pengfei Ge, Jianmin Liang

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
6.2field-weighted citation impact, top 3% 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

43 citing papers in PubMed, 94 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 3 institutions in 1 country.

Tianfei LuoDepartment of Neurology, First Hospital of Jilin University, Changchun 130021, China. luotianfei2010@126.com.
Guiying LiuDepartment of Pediatrics, Anzhen Hospital of Capital University of Medical Sciences, Beijing 10029, China. liugvying@126.com.
Hongxi MaDepartment of Pathology, First Hospital of Jilin University, Changchun 130021, China. mahongxi1969@163.com.
Bin LuDepartment of Neurosurgery, First Hospital of Jilin University, Changchun 130021, China. Lubin03216@163.com.
Haiyang XuDepartment of Neurosurgery, First Hospital of Jilin University, Changchun 130021, China. xuhaiyang76@163.com.
Yujing WangDepartment of Pediatrics, First Hospital of Jilin University, Changchun 130021, China. yujingwang2012@126.com.
Jiang WuDepartment of Neurology, First Hospital of Jilin University, Changchun 130021, China. drwujiang2010@163.com.
Pengfei GeDepartment of Neurosurgery, First Hospital of Jilin University, Changchun 130021, China. pengfeige@gmail.com.
Jianmin LiangDepartment of Pediatrics, First Hospital of Jilin University, Changchun 130021, China. jakcyliangjm@163.com.
Jilin University · CNFirst Hospital of Jilin University · CNBeijing Anzhen Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lethal autophagy is a pathway leading to neuronal death caused by transient global ischemia. In this study, we examined the effect of Ginsenoside Rb1 (GRb1) on ischemia/reperfusion-induced autophagic neuronal death and investigated the role of PI3K/Akt. Ischemic neuronal death in vitro was induced by using oxygen glucose deprivation (OGD) in SH-SY5Y cells, and transient global ischemia was produced by using two vessels occlusion in rats. Cellular viability of SH-SY5Y cells was assessed by MTT assay, and CA1 neuronal death was evaluated by Hematoxylin-eosin staining. Autophagic vacuoles were detected by using both fluorescent microscopy in combination with acridine orange (AO) and Monodansylcadaverine (MDC) staining and transmission electronic microscopy. Protein levels of LC3II, Beclin1, total Akt and phosphor-Akt at Ser473 were examined by western blotting analysis. GRb1 inhibited both OGD and transient ischemia-induced neuronal death and mitigated OGD-induced autophagic vacuoles in SH-SY5Y cells. By contrast, PI3K inhibitor LY294002 counteracted the protection of GRb1 against neuronal death caused by either OGD or transient ischemia. LY294002 not only mitigated the up-regulated protein level of phosphor Akt at Ser473 caused by GRb1, but also reversed the inhibitory effect of GRb1 on OGD and transient ischemia-induced elevation in protein levels of LC3II and Beclin1.

Indexed as

PhytotherapyAnimalsApoptosis Regulatory ProteinsAutophagyBeclin-1Brain IschemiaCA1 Region, HippocampalCell Line, TumorChromonesEnzyme ActivationGinsenosidesGlucoseHumansMaleMicrotubule-Associated ProteinsMorpholines2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-oneAnxa3 protein, ratApoptosis Regulatory ProteinsBeclin-1Becn1 protein, ratChromonesginsenoside Rb1GinsenosidesGlucoseMicrotubule-Associated ProteinsMorpholinesNerve Tissue ProteinsNeuroprotective AgentsOxygenPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-akt

Identifiers

PMID25257523
PMCPMC4200757
OpenAlexW2161706084

What OpenQuestion holds

Textmetadata
LicenceCC BY
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 OpenQuestion graph.