Evidence map›Paper›PMID 30905926›Full record

Trial reportMedical science monitor : international medical journal of experimental and clinical research2019

Neuro-Protective Role of Metformin in Patients with Acute Stroke and Type 2 Diabetes Mellitus via AMPK/Mammalian Target of Rapamycin (mTOR) Signaling Pathway and Oxidative Stress.

Min Zhao, Xiao Wan Li, De Z Chen, Fang Hao, Shu X Tao, Hai Yan Yu, Rui Cheng, Hong Liu

Open access · hybridAbstract readRandomized Controlled Trial
PubMed Full text at PMC Publisher
In one paragraph

Trial report in Medical science monitor : international medical journal of experimental and clinical research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed, 2 pooled it
4.6field-weighted citation impact, top 5% 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

51 citing papers in PubMed, 2 syntheses or guidelines pooled it, 97 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

8 authors at 1 institution in 1 country.

Min ZhaoDepartment of Neurology, Liaocheng People's Hospital, Liaocheng, Shandong, China (mainland).
Xiao Wan LiDepartment of Neurology, Liaocheng People's Hospital, Liaocheng, Shandong, China (mainland).
De Z ChenDepartment of Neurology, Liaocheng People's Hospital, Liaocheng, Shandong, China (mainland).
Fang HaoDepartment of Neurology, Liaocheng People's Hospital, Liaocheng, Shandong, China (mainland).
Shu X TaoDepartment of Neurology, Liaocheng People's Hospital, Liaocheng, Shandong, China (mainland).
Hai Yan YuDepartment of Neurology, Liaocheng People's Hospital, Liaocheng, Shandong, China (mainland).
Rui ChengGovernment Clinics of Liaocheng, Liaocheng, Shandong, China (mainland).
Hong LiuDepartment of Neurology, Liaocheng People's Hospital, Liaocheng, Shandong, China (mainland).
Liaocheng People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND We investigated the effects of metformin on neurological function and oxidative stress in patients with type 2 diabetes mellitus with acute stroke. MATERIAL AND METHODS We randomly assigned 80 acute stroke patients to 2 groups: the metformin combined group and the insulin group. Each group had 40 patients and all were treated with standard stroke treatment. The indexes of nervous functional score and oxidative stress were measured before and 2 weeks after treatment. The primary fetal rat hippocampal neurons were gradually matured after 7 days of culture, and divided into the control group (Con), the oxygen-glucose deprivation model group (Mod), and the metformin group (Met). In the Met group, 10 mmol/L metformin was added, and the Con group and the Mod group received equal volumes of cell culture fluid. Cell viability, cell apoptosis rate, and the expression of Bax, Bcl-2, AMPK, pAMPK and mTOR were detected; MDA content and SOD activity were also detected. RESULTS Before treatment, there was no difference in the metrical indexes between the 2 groups. After treatment, the treatment group was better than the control group in neurological function scores and multiple oxidative stress-related indicators. The experimental results of primary fetal rat hippocampal neuronal cells suggest that this mechanism of improvement is closely related to the AMPK/mTOR signaling pathway. CONCLUSIONS Metformin can improve the neurological function and oxidative stress status of acute stroke patients with type 2 diabetes, and its mechanism may be related to the AMPK/mTOR signaling pathway and oxidative stress.

Indexed as

AdultAgedAMP-Activated Protein KinasesAnimalsApoptosisCell SurvivalDiabetes Mellitus, Type 2FemaleHippocampusHumansHypoglycemic AgentsInsulinMaleMetforminMiddle AgedNeuronsAMP-Activated Protein KinasesHypoglycemic AgentsInsulinMetforminMTOR protein, humanmTOR protein, ratNeuroprotective AgentsTOR Serine-Threonine Kinases

Identifiers

PMID30905926
PMCPMC6442495
OpenAlexW2988173536

What OpenQuestion holds

Texttitle and abstract
LicenceCC BY-NC-ND
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.