Evidence map›Paper›PMID 26254913›Full record

ArticleJournal of molecular neuroscience : MN2015

The Protective Effect of Remote Renal Preconditioning Against Hippocampal Ischemia Reperfusion Injury: Role of KATP Channels.

Fatemeh Zare Mehrjerdi, Nahid Aboutaleb, Hamidreza Pazoki-Toroudi, Mansoureh Soleimani, Marjan Ajami, Mehdi Khaksari, Fatemeh Safari, Rouhollah Habibey

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of molecular neuroscience : MN, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.6field-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

19 citing papers in PubMed, 39 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 5 institutions in 2 countries.

Fatemeh Zare MehrjerdiDepartment of Physiology, School of Medicine, Shahid Sadoughi University of Medical Sciences, Yazd, Iran.
Nahid AboutalebPhysiology Research Center, Physiology Department, Faculty of Medicine, Iran University of Medical Sciences, Tehran, Iran. dr.nabotaleb@gmail.com.
Hamidreza Pazoki-ToroudiPhysiology Research Center, Physiology Department, Faculty of Medicine, Iran University of Medical Sciences, Tehran, Iran.
Mansoureh SoleimaniCellular and Molecular Research Center, Faculty of Medicine, Iran University of Medical Sciences, Tehran, Iran.
Marjan AjamiNational Nutrition and Food Technology Research Institute, Faculty of Nutrition Science and Food Technology, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Mehdi KhaksariDepartment of Physiology, School of Medicine, Shahroud University of Medical Sciences, Shahroud, Iran.
Fatemeh SafariDepartment of Physiology, School of Medicine, Shahid Sadoughi University of Medical Sciences, Yazd, Iran.
Rouhollah HabibeyDepartment of Neuroscience and Brain Technologies, Istituto Italiano di Technologia, Via Morego 30, Genova, 16163, Italy.
Iran University of Medical Sciences · IRShahid Sadoughi University of Medical Sciences and Health Services · IRItalian Institute of Technology · ITShahid Beheshti University of Medical Sciences · IRShahroud University of Medical Sciences · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Remote ischemic preconditioning (RIPC), which consists of several brief ischemia/reperfusion applied at the remote site of lethal ischemia reperfusion, can, through activating different mechanisms, increase the ability of the body's endogenous protection against prolonged ischemia/reperfusion. Recent studies have shown that RIPC has neuroprotective effects, but its mechanisms are not well elucidated. The present study aimed to determine whether activation of KATP channels in remote renal preconditioning decreases hippocampus damage induced by global cerebral ischemia. RIPC was induced by ischemia of the left renal artery (IPC); 24 h later, global cerebral ischemia reperfusion (IR) was induced by common carotid arteries occlusion. 5hydroxydecanoate (5HD) and glibenclamide (Gli) were injected before of IPC. The levels of malondialdehyde (MDA) and catalase (CAT) activity were assessed in hippocampus. Terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) was assessed to detect apoptotic cells in hippocampus. RIPC inhibited apoptosis by decreasing positive TUNEL cells (P < 0.05). KATP channels blocking with 5HD and Gli markedly increased apoptosis in hippocampal cells in RIPC group (P < 0.001). RIPC decreased MDA level and increased CAT activity in ischemic hippocampus (P < 0.01). Also, 5HD and Gli inhibited the effect of RIPC on MDA level and CAT activity (P < 0.05). The present study shows that RIPC can effectively attenuate programmed cell death, increase activity of CAT, and reduce MDA levels. Blocking of KATP channels inhibited the protective effects of RIPC.

Indexed as

AnimalsApoptosisCatalaseDecanoic AcidsGlyburideHippocampusHydroxy AcidsIschemic PreconditioningKATP ChannelsKidneyMaleMalondialdehydeMiceMice, Inbred BALB CPotassium Channel BlockersReperfusion Injury5-hydroxydecanoic acidCatalaseDecanoic AcidsGlyburideHydroxy AcidsKATP ChannelsMalondialdehydePotassium Channel BlockersApoptosisHippocampusKATP channelsRemote ischemic preconditioning

Identifiers

PMID26254913
OpenAlexW1842300473

What OpenQuestion holds

Textmetadata
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.