Evidence map›Paper›PMID 37740074›Full record

ReviewCellular and molecular neurobiology2023

The Impact of Cerebral Ischemia on Antioxidant Enzymes Activity and Neuronal Damage in the Hippocampus.

Jafar Sadeghzadeh, Leila Hosseini, Ahmad Mobed, Hamid Soltani Zangbar, Jaber Jafarzadeh, Jamshid Pasban, Parviz Shahabi

Open access · greenAbstract readReview
In one paragraph

Review in Cellular and molecular neurobiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
2.3field-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

15 citing papers in PubMed, 1 synthesis or guideline pooled it, 19 citations in OpenAlex.

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  8. Extract ofInternational journal of molecular sciences · 2025
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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

7 authors at 1 institution in 1 country.

Jafar SadeghzadehDepartment of Neuroscience and Cognition, Faculty of Advanced Medical Sciences, Tabriz University of Medical Sciences, Tabriz, Islamic Republic of Iran.ORCID http://orcid.org/0000-0002-7632-4162
Leila HosseiniResearch Center of Psychiatry and Behavioral Sciences, Tabriz University of Medical Sciences, Tabriz, Islamic Republic of Iran.ORCID http://orcid.org/0000-0002-4203-4618
Ahmad MobedPhysical Medicine and Rehabilitation Research Center, Tabriz University of Medical Sciences, Tabriz, Islamic Republic of Iran.ORCID http://orcid.org/0000-0001-8939-3688
Hamid Soltani ZangbarDepartment of Neuroscience and Cognition, Faculty of Advanced Medical Sciences, Tabriz University of Medical Sciences, Tabriz, Islamic Republic of Iran.ORCID http://orcid.org/0000-0001-6979-0723
Jaber JafarzadehDepartment of Community Nutrition Faculty of Nutrition and Food Science, Tabriz University of Medical Sciences, Tabriz, Islamic Republic of Iran.ORCID http://orcid.org/0000-0001-6795-2952
Jamshid PasbanDepartment of Neuroscience and Cognition, Faculty of Advanced Medical Sciences, Tabriz University of Medical Sciences, Tabriz, Islamic Republic of Iran.
Parviz ShahabiDepartment of Physiology, School of Medicine, Tabriz University of Medical Sciences, Tabriz, Islamic Republic of Iran. Shahabip@tbzmed.ac.ir.ORCID http://orcid.org/0000-0001-5594-5544
Tabriz University of Medical Sciences · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cerebral ischemia and subsequent reperfusion, leading to reduced blood supply to specific brain areas, remain significant contributors to neurological damage, disability, and mortality. Among the vulnerable regions, the subcortical areas, including the hippocampus, are particularly susceptible to ischemia-induced injuries, with the extent of damage influenced by the different stages of ischemia. Neural tissue undergoes various changes and damage due to intricate biochemical reactions involving free radicals, oxidative stress, inflammatory responses, and glutamate toxicity. The consequences of these processes can result in irreversible harm. Notably, free radicals play a pivotal role in the neuropathological mechanisms following ischemia, contributing to oxidative stress. Therefore, the function of antioxidant enzymes after ischemia becomes crucial in preventing hippocampal damage caused by oxidative stress. This study explores hippocampal neuronal damage and enzymatic antioxidant activity during ischemia and reperfusion's early and late stages.

Indexed as

Brain IschemiaReperfusion InjuryAntioxidantsFree RadicalsHippocampusHumansIschemiaOxidative StressAntioxidantsFree RadicalsAntioxidant enzymesCerebral ischemiaHippocampusNeuronal damageOxidative stress

Identifiers

PMID37740074
PMCPMC11407731
OpenAlexW4386949869

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.