Evidence map›Paper›PMID 34343971›Full record

ArticleAging2021

The protective effect of allicin on myocardial ischemia-reperfusion by inhibition of Ca

Tong Gao, Peng Yang, Dongliang Fu, Mengru Liu, Xinyi Deng, Mingjing Shao, Jiangquan Liao, Hong Jiang, Xianlun Li

Open access · hybridAbstract read
In one paragraph

Article in Aging, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing 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

17 citing papers in PubMed, 22 citations in OpenAlex.

  1. Review
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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.

Tong GaoGraduate School of Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing 100730, China.
Peng YangDepartment of Integrative Medicine Cardiology, China-Japan Friendship Hospital, Beijing 100029, China.
Dongliang FuDepartment of Integrative Medicine Cardiology, China-Japan Friendship Hospital, Beijing 100029, China.
Mengru LiuGraduate School of Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing 100730, China.
Xinyi DengDepartment of Integrative Medicine Cardiology, China-Japan Friendship Hospital, Beijing 100029, China.
Mingjing ShaoDepartment of Integrative Medicine Cardiology, China-Japan Friendship Hospital, Beijing 100029, China.
Jiangquan LiaoDepartment of Integrative Medicine Cardiology, China-Japan Friendship Hospital, Beijing 100029, China.
Hong JiangDepartment of Integrative Medicine Cardiology, China-Japan Friendship Hospital, Beijing 100029, China.
Xianlun LiGraduate School of Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing 100730, China.
China-Japan Friendship Hospital · CNChinese Academy of Medical Sciences & Peking Union Medical College · CNPeking University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeTo investigate the protective effect and mechanism of allicin on myocardial ischemia-reperfusion (MI/R) injury.

methodsWe investigated the mechanisms by which allicin attenuated the MI/R injury by focusing on phosphoinositide 3-kinase, G protein coupled receptor kinases 2, phospholipase Cγ and cardiomyocyte apoptosis. Sixty male mice were randomly assigned into three groups: repeated MI/R (model), sham-operated (control), and MI/R+ allicin group (allicin). Ultrasound examination was used to examine the cardiac function. Masson staining was used to evaluate the myocardial infarct area. TUNEL assay was performed to examine the anti-apoptotic effect of allicin. Differentially expressed genes (DEGs) and pathways were analyzed by mRNA microarray analysis. Immunofluorescence staining and western blot were carried out to detect the effect of allicin on the PI3K. A pan-PLC activator, m-3M3FBS, was applied to investigate whether allicin induced cardiomyocyte apoptosis was via the GRK2/PLC/IP3R signaling pathway.

resultsMasson staining and the TUNEL assay revealed that allicin reduced infarct size and played an anti-apoptotic role in M/IR. Ultrasound examination revealed that allicin improved cardiac function after M/IR injury. Gene ontology analysis indicated that the calcium signaling pathway and PI3KCA(PI3K) were selected. Immunofluorescence staining and western blot exposed that PI3K was activated by allicin during MI/R injury. Fura-2AM staining revealed that the PI3K -mediated GRK2/PLC-γ/IP3R pathway may be involved in the protective effect of allicin on MI/R injury.

conclusionsAllicin has a protective effect on MI/R injury. This effect might be associated with the inhibition of Ca

Indexed as

AdenosylhomocysteinaseAnimalsApoptosisCalcium SignalingDisulfidesG-Protein-Coupled Receptor Kinase 2MaleMiceMyocardial InfarctionMyocardial IschemiaMyocardial Reperfusion InjuryMyocytes, CardiacPhosphatidylinositol 3-KinasesPhospholipase C gammaRatsRats, WistarAdenosylhomocysteinaseallicinDisulfidesG-Protein-Coupled Receptor Kinase 2Phosphatidylinositol 3-KinasesPhospholipase C gammaSulfinic Acidsallicinapoptosiscalcium signaling pathwaygene expression profilingGPCRGRK2myocardial ischemia/reperfusionPI3K/Akt pathway

Identifiers

PMID34343971
PMCPMC8386544
OpenAlexW3189904166

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.