Evidence map›Paper›PMID 32466476›Full record

ArticleBiomolecules2020

Post-Treatment of Synthetic Polyphenolic 1,3,4 Oxadiazole Compound A3, Attenuated Ischemic Stroke-Induced Neuroinflammation and Neurodegeneration.

Arooj Mohsin Alvi, Lina Tariq Al Kury, Muhammad Umar Ijaz, Fawad Ali Shah, Muhammad Tariq Khan, Ahmed Sadiq Sheikh, Humaira Nadeem, Arif-Ullah Khan, Alam Zeb, Shupeng Li

Open access · goldAbstract read
In one paragraph

Article in Biomolecules, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.6field-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

27 citing papers in PubMed, 56 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

10 authors at 4 institutions in 3 countries.

Arooj Mohsin AlviRiphah Institute of Pharmaceutical Sciences, Riphah International University, Islamabad 44000, Pakistan.
Lina Tariq Al KuryCollege of Natural and Health Sciences, Zayed University, Abu Dhabi 144534, UAE.
Muhammad Umar IjazDepartment of Zoology, Wildlife, and Fisheries, University of Agriculture, Faisalabad 38000, Pakistan.
Fawad Ali ShahRiphah Institute of Pharmaceutical Sciences, Riphah International University, Islamabad 44000, Pakistan.
Muhammad Tariq KhanRiphah Institute of Pharmaceutical Sciences, Riphah International University, Islamabad 44000, Pakistan.
Ahmed Sadiq SheikhRiphah Institute of Pharmaceutical Sciences, Riphah International University, Islamabad 44000, Pakistan.
Humaira NadeemRiphah Institute of Pharmaceutical Sciences, Riphah International University, Islamabad 44000, Pakistan.
Arif-Ullah KhanRiphah Institute of Pharmaceutical Sciences, Riphah International University, Islamabad 44000, Pakistan.
Alam ZebRiphah Institute of Pharmaceutical Sciences, Riphah International University, Islamabad 44000, Pakistan.
Shupeng LiState Key Laboratory of Oncogenomics, School of Chemical Biology and Biotechnology, Shenzhen Graduate School, Peking University, Shenzhen 518055, China.
Riphah International University · PKPeking University · CNUniversity of Agriculture Faisalabad · PKZayed University · AE

Funding

HEC Pakistan, Peking University China HEC Pakistan, Peking University China
6 · The paper itself

Abstract

Ischemic stroke is categorized by either permanent or transient blood flow obstruction, impeding the distribution of oxygen and essential nutrients to the brain. In this study, we examined the neuroprotective effects of compound A3, a synthetic polyphenolic drug product, against ischemic brain injury by employing an animal model of permanent middle cerebral artery occlusion (p-MCAO). Ischemic stroke induced significant elevation in the levels of reactive oxygen species and, ultimately, provoked inflammatory cascade. Here, we demonstrated that A3 upregulated the endogenous antioxidant enzymes, such as glutathione s-transferase (GST), glutathione (GSH), and reversed the ischemic-stroke-induced nitric oxide (NO) and lipid peroxidation (LPO) elevation in the peri-infarct cortical and striatal tissue, through the activation of endogenous antioxidant nuclear factor E2-related factor or nuclear factor erythroid 2 (Nrf2). In addition, A3 attenuated neuroinflammatory markers such as ionized calcium-binding adapter molecule-1 (Iba-1), cyclooxygenase-2 (COX-2), tumor necrotic factor-α (TNF-α), toll-like receptors (TLR4), and nuclear factor-κB (NF-κB) by down-regulating p-JNK as evidenced by immunohistochemical results. Moreover, treatment with A3 reduced the infarction area and neurobehavioral deficits. We employed ATRA to antagonize Nrf2, which abrogated the neuroprotective effects of A3 to further assess the possible involvement of the Nrf2 pathway, as demonstrated by increased infarction and hyperexpression of inflammatory markers. Together, our findings suggested that A3 could activate Nrf2, which in turn regulates the downstream antioxidants, eventually mitigating MCAO-induced neuroinflammation and neurodegeneration.

Indexed as

AnimalsAntioxidantsBrain IschemiaInflammationIschemic StrokeMaleMolecular StructureNeuroprotective AgentsOxadiazolesOxidative StressRatsRats, Sprague-Dawley1,3,4-oxadiazoleAntioxidantsNeuroprotective AgentsOxadiazolesA3all-trans retinoic acidantioxidant systemmiddle cerebral artery occlusionneurodegeneration

Identifiers

PMID32466476
PMCPMC7355474
OpenAlexW3030099697

What OpenQuestion holds

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LicenceCC BY
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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.