Evidence mapPaperPMID 29671019Full record

ArticleNaunyn-Schmiedeberg's archives of pharmacology2018

Lixisenatide, a novel GLP-1 analog, protects against cerebral ischemia/reperfusion injury in diabetic rats.

Rania G Abdel-Latif, Gehan H Heeba, Ashraf Taye, Mohamed M A Khalifa

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Article in Naunyn-Schmiedeberg's archives of pharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
2.8field-weighted citation impact, top 10% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.

  1. Pooled it
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  8. Therapeutic Efficacy ofPharmaceuticals (Basel, Switzerland) · 2024
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  18. Glucagon-like peptide-1 receptor agonists as neuroprotective agents for ischemic stroke: a systematic scoping review.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2021
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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

4 authors at 1 institution in 1 country.

Rania G Abdel-LatifDepartment of Pharmacology and Toxicology, Faculty of Pharmacy, Minia University, El-Minia, 61111, Egypt.
Gehan H HeebaDepartment of Pharmacology and Toxicology, Faculty of Pharmacy, Minia University, El-Minia, 61111, Egypt. gehan_heeba@mu.edu.eg.
Ashraf TayeDepartment of Pharmacology and Toxicology, Faculty of Pharmacy, Minia University, El-Minia, 61111, Egypt.
Mohamed M A KhalifaDepartment of Pharmacology and Toxicology, Faculty of Pharmacy, Minia University, El-Minia, 61111, Egypt.
Minia University · EG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Type 2 diabetes mellitus (T2DM) is a major risk factor for ischemic stroke accompanied by vascular dysfunction and poor cerebrovascular outcome. Lixisenatide is a glucagon like peptide-1 (GLP-1) analog that is recently used for T2DM treatment with established neuroprotective properties. This study investigated and compared the neuroprotective effect of lixisenatide against glimepiride on diabetic rats subjected to global cerebral ischemia/reperfusion (I/R) injury. T2DM-induced adult male Wistar rats were administered lixisenatide or glimepiride prior to induction of global cerebral I/R-induced injury. Results showed a disturbance in oxidative stress parameters (catalase, reduced glutathione, and malondialdehyde) along with increasing in caspase-3 and tumor necrosis factor-alpha protein expressions in ischemic diabetic brain tissues. An upregulation of protein level of inducible nitric oxide (iNOS) synthase and nicotinamide adenine dinucleotide phosphate (NADPH) oxidase subunit, NOX2 gene expression associated with significant suppression of endothelial nitric oxide synthase (eNOS) protein expression are recorded in carotid arteries of diabetic I/R-injured rats. Apart from ameliorating glucose intolerance and insulin resistance, lixisenatide was found to be superior to glimepiride as protective treatment in terms of enhancing behavioral/neurological functions and suppressing cerebral oxidative stress, inflammation, and apoptosis in cerebral I/R-injured diabetic rats. Unlike glimepiride, lixisenatide relieved carotid endothelial dysfunction by increasing eNOS expression. It also dampened vascular nitrosative/oxidative stress via suppression of iNOS and NADPH oxidase expressions. This study supposed that lixisenatide represents a more suitable anti-diabetic therapy for patients who are at risk of ischemic stroke, and even so, the mechanisms of lixisenatide-mediated vascular protection warrant further experimental and clinical investigations.

Indexed as

AnimalsBrain IschemiaCarotid ArteriesDiabetes Mellitus, ExperimentalGlucagon-Like Peptide 1Glucagon-Like Peptide-2 ReceptorHypoglycemic AgentsInsulin ResistanceMaleNADPH Oxidase 2NADPH OxidasesNeuroprotective AgentsNitric Oxide Synthase Type IINitric Oxide Synthase Type IIIOxidative StressPeptidesCybb protein, ratGlucagon-Like Peptide 1Glucagon-Like Peptide-2 ReceptorHypoglycemic AgentslixisenatideNADPH Oxidase 2NADPH OxidasesNeuroprotective AgentsNitric Oxide Synthase Type IINitric Oxide Synthase Type IIINos2 protein, ratNos3 protein, ratPeptidesCerebral ischemia/reperfusionGlimepirideGLP-1LixisenatideType 2 diabetes mellitusVascular injury

Identifiers

PMID29671019
OpenAlexW2800054720

What Socratic holds

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Read underepoch 390

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 Socratic graph.