Evidence map›Paper›PMID 25237906›Full record

ArticlePloS one2014

Tetramethylpyrazine suppresses transient oxygen-glucose deprivation-induced connexin32 expression and cell apoptosis via the ERK1/2 and p38 MAPK pathway in cultured hippocampal neurons.

Gu Gong, Libang Yuan, Lin Cai, Maorong Ran, Yulan Zhang, Huaqu Gong, Xuemei Dai, Wei Wu, Hailong Dong

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

16 citing papers in PubMed, 35 citations in OpenAlex.

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  11. Tetramethylpyrazine Protects Neurons from Oxygen-Glucose Deprivation-Induced Death.Medical science monitor : international medical journal of experimental and clinical research · 2017
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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

9 authors at 3 institutions in 1 country.

Gu GongDepartment of Anesthesia, General Hospital of Chengdu Military Area Command, Chengdu, Sichuan, China.
Libang YuanDepartment of Anesthesia, General Hospital of Chengdu Military Area Command, Chengdu, Sichuan, China.
Lin CaiDepartment of Anesthesia, General Hospital of Chengdu Military Area Command, Chengdu, Sichuan, China.
Maorong RanDepartment of Anesthesia, General Hospital of Chengdu Military Area Command, Chengdu, Sichuan, China.
Yulan ZhangDepartment of Anesthesia, General Hospital of Chengdu Military Area Command, Chengdu, Sichuan, China.
Huaqu GongDepartment of Anesthesia, General Hospital of Chengdu Military Area Command, Chengdu, Sichuan, China.
Xuemei DaiDepartment of Anesthesia, General Hospital of Chengdu Military Area Command, Chengdu, Sichuan, China.
Wei WuDepartment of Anesthesia, General Hospital of Chengdu Military Area Command, Chengdu, Sichuan, China.
Hailong DongDepartment of Anesthesia, the Fourth Military Medical University Xijing Hospital, Xi'an, Shaanxi, China.
Kunming General Hospital of Chengdu Military Command · CNChengdu Military General Hospital · CNXijing Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tetramethylpyrazine (TMP) has been widely used in China as a drug for the treatment of various diseases. Recent studies have suggested that TMP has a protective effect on ischemic neuronal damage. However, the exact mechanism is still unclear. This study aims to investigate the mechanism of TMP mediated ischemic hippocampal neurons injury induced by oxygen-glucose deprivation (OGD). The effect of TMP on hippocampal neurons viability was detected by MTT assay, LDH release assay and apoptosis rate was measured by flow cytometry. TMP significantly suppressed neuron apoptosis in a concentration-dependent manner. TMP could significantly reduce the elevated levels of connexin32 (Cx32) induced by OGD. Knockdown of Cx32 by siRNA attenuated OGD injury. Moreover, our study showed that viability was increased in siRNA-Cx32-treated-neurons, and neuron apoptosis was suppressed by activating Bcl-2 expression and inhibiting Bax expression. Over expression of Cx32 could decrease neurons viability and increase LDH release. Furthermore, OGD increased phosphorylation of ERK1/2 and p38, whose inhibitors relieved the neuron injury and Cx32 up-regulation. Taken together, TMP can reverse the OGD-induced Cx32 expression and cell apoptosis via the ERK1/2 and p38 MAPK pathways.

Indexed as

AnimalsApoptosisCells, CulturedConnexinsGap Junction beta-1 ProteinGene Expression RegulationGene Knockdown TechniquesGlucoseHippocampusMAP Kinase Signaling SystemNeuronsOxygenPhosphorylationPyrazinesRats, WistarRNA InterferenceConnexinsGap Junction beta-1 ProteinGlucoseOxygenPyrazinestetramethylpyrazine

Identifiers

PMID25237906
PMCPMC4169508
OpenAlexW2035254220

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.