Evidence map›Paper›PMID 32210331›Full record

ArticleScientific reports2020

RIPC provides neuroprotection against ischemic stroke by suppressing apoptosis via the mitochondrial pathway.

Jing Lv, Weikang Guan, Qiang You, Li Deng, Yan Zhu, Kan Guo, Xiaoqing Gao, Jiming Kong, Chaoxian Yang

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 2 pooled it
3.7field-weighted citation impact, top 6% 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

31 citing papers in PubMed, 2 syntheses or guidelines pooled it, 53 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

9 authors at 3 institutions in 2 countries.

Jing Lv *Department of Neurobiology, Preclinical Medicine Research Center, Southwest Medical University, Luzhou, 646000, China.
Weikang Guan *Department of Neurobiology, Preclinical Medicine Research Center, Southwest Medical University, Luzhou, 646000, China.
Qiang You *Department of Nuclear Medicine, Affiliated Hospital of Southwest Medical University & Nuclear Medicine and Molecular Imaging Key Laboratory of Sichuan province, Luzhou, 646000, China.
Li DengDepartment of Neurobiology, Preclinical Medicine Research Center, Southwest Medical University, Luzhou, 646000, China.
Yan ZhuDepartment of Anatomy, College of Basic Medicine, Southwest Medical University, Luzhou, 646000, China.
Kan GuoDepartment of Neurobiology, Preclinical Medicine Research Center, Southwest Medical University, Luzhou, 646000, China.
Xiaoqing GaoDepartment of Neurobiology, Preclinical Medicine Research Center, Southwest Medical University, Luzhou, 646000, China.
Jiming KongDepartment of Neurobiology, Preclinical Medicine Research Center, Southwest Medical University, Luzhou, 646000, China. Jiming.Kong@umanitoba.ca.
Chaoxian YangDepartment of Neurobiology, Preclinical Medicine Research Center, Southwest Medical University, Luzhou, 646000, China. lyycx@foxmail.com.
Southwest Medical University · CNAffiliated Hospital of Southwest Medical University · CNThe First People's Hospital of Guiyang · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ischemic stroke is a common disease with high morbidity and mortality. Remote ischemic preconditioning (RIPC) can stimulate endogenous protection mechanisms by inducing ischemic tolerance to reduce subsequent damage caused by severe or fatal ischemia to non-ischemic organs. This study was designed to assess the therapeutic properties of RIPC in ischemic stroke and to elucidate their underlying mechanisms. Neurobehavioral function was evaluated with the modified neurological severity score (mNSS) test and gait analysis. PET/CT was used to detect the ischemic volume and level of glucose metabolism. The protein levels of cytochrome c oxidase-IV (COX-IV) and heat shock protein 60 (HSP60) were tested by Western blotting. TUNEL and immunofluorescence staining were used to analyze apoptosis and to observe the nuclear translocation and colocalization of apoptosis-inducing factor (AIF) and endonuclease G (EndoG) in apoptotic cells. Transmission electron microscopy (TEM) was used to detect mitochondrial-derived vesicle (MDV) production and to assess mitochondrial ultrastructure. The experimental results showed that RIPC exerted significant neuroprotective effects, as indicated by improvements in neurological dysfunction, reductions in ischemic volume, increases in glucose metabolism, inhibition of apoptosis, decreased nuclear translocation of AIF and EndoG from mitochondria and improved MDV formation. In conclusion, RIPC alleviates ischemia/reperfusion injury after ischemic stroke by inhibiting apoptosis via the endogenous mitochondrial pathway.

Indexed as

AnimalsApoptosisApoptosis Inducing FactorBrainChaperonin 60Electron Transport Complex IVEndodeoxyribonucleasesGaitGlucoseIschemic PreconditioningIschemic StrokeMice, Inbred C57BLMitochondriaMitochondrial ProteinsNeuroprotectionPositron Emission Tomography Computed TomographyApoptosis Inducing FactorChaperonin 60Electron Transport Complex IVEndodeoxyribonucleasesendonuclease GGlucoseHspd1 protein, mouseMitochondrial Proteins

Identifiers

PMID32210331
PMCPMC7093414
OpenAlexW3013660715

What OpenQuestion holds

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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.