Evidence map›Paper›PMID 30269302›Full record

ArticleMetabolic brain disease2019

Protective effects of Nesfatin-1 peptide on cerebral ischemia reperfusion injury via inhibition of neuronal cell death and enhancement of antioxidant defenses.

Sohaila Erfani, Ali Moghimi, Nahid Aboutaleb, Mehdi Khaksari

Abstract read
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In one paragraph

Article in Metabolic brain disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
–field-weighted citation impact
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. Article
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  3. Review
  4. The role of amphipathic and cationic helical peptides in Parkinson's disease.Protein science : a publication of the Protein Society · 2025
    Review
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  8. Article
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  13. Xuan Bi Tong Yu Fang Promotes Angiogenesis via VEGF-Notch1/Dll4 Pathway in Myocardial Ischemic Rats.Evidence-based complementary and alternative medicine : eCAM · 2020
    Article
  14. The association of low levels of nesfatin-1 and glucagon-like peptide-1 with oxidative stress in Parkinson's disease.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2019
    Article
  15. Review
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

4 authors.

Sohaila ErfaniDepartment of Biology, Faculty of Science, Ferdowsi University of Mashhad, Mashhad, Iran.
Ali MoghimiRayan Center for Neuroscience and Behavior, Department of Biology, Faculty of Science, Ferdowsi University of Mashhad, Mashhad, Iran.
Nahid AboutalebPhysiology Research Center, Faculty of Medicine, Iran University of Medical Sciences, Tehran, Iran. dr.nabotaleb@gmail.com.
Mehdi KhaksariAddiction Research Center, Shahroud University of Medical Sciences, Shahroud, Iran.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nesfatin-1 is a novel peptide with anorexigenic and anti-hyperglycemic properties. According to previous studies, this multi-functional peptide protects dopaminergic cells against neurotoxicity via anti-apoptotic effects. In addition, Nesfatin-1 protects myocardial tissue after myocardial infarction via anti-inflammatory and anti-apoptotic mechanisms. In this study, we investigated the neuroprotective effects of nesfatin-1 against cerebral ischemia reperfusion injury in the CA1 area of hippocampus in rats. 56 male Wistar rats (240-270 g) were randomly selected and allocated into four groups: (1) sham, (2) nesfatin-1, (3) ischemia/reperfusion, (4) ischemia/reperfusion+nesfatin-1. Cerebral ischemia induced by the occlusion of the common carotid arteries for 20 min was followed by reperfusion. Saline as a vehicle and nesfatin-1 (20 μg/kg) were injected intraperitoneally (IP) at the start of cerebral reperfusion. Apoptotic and necrotic cell death was detected by TUNEL and Nissl staining. Malondialdehyde (MDA) and antioxidant enzymes (GSH and SOD) levels were measured by the ELISA method. The results showed that cerebral ischemia increased the apoptotic and necrotic cell death in the CA1 area of hippocampus, while, treatment with nesfatin-1significantly reduced apoptotic and necrotic cell death. Moreover, the MDA levels of the hippocampus in ischemic rats were higher, whereas in nesfatin-1-treated rats the MDA levels were decreased. Furthermore, the SOD and GSH levels in the ischemic rats were decreased, whilst in ischemic rats treated with nesfatin-1, the SOD and GSH levels were increased. This study for the first time found that nesfatin-1 treatment improves CA1 hippocampus injuries after cerebral ischemia through preventing neuronal cell death and enhancement of antioxidant defenses.

Indexed as

AnimalsAntioxidantsApoptosisCalcium-Binding ProteinsCaspase 3Cell DeathDisease Models, AnimalDNA-Binding ProteinsHippocampusMaleMalondialdehydeNerve Tissue ProteinsNeuronsNeuroprotective AgentsNucleobindinsOxidative StressAntioxidantsCalcium-Binding ProteinsCaspase 3DNA-Binding ProteinsMalondialdehydeNerve Tissue ProteinsNeuroprotective AgentsNucb1 protein, ratNucleobindinsSuperoxide DismutaseApoptosisBrain ischemiaHippocampusNecrosisNesfatin-1

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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.