Evidence map›Paper›PMID 29909460›Full record

ArticleNaunyn-Schmiedeberg's archives of pharmacology2018

Modulation of brain ACE and ACE2 may be a promising protective strategy against cerebral ischemia/reperfusion injury: an experimental trial in rats.

Maha Mohammed Abdel-Fattah, Basim Anwar Shehata Messiha, Ahmed Mohamed Mansour

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In one paragraph

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 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
3.4field-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

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

  1. Pooled it
  2. Review
  3. Article
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  6. Review
  7. Article
  8. Protective Effect of Nimodipine Against Valproic-acid Induced Biochemical and Behavioral Phenotypes of Autism.Clinical psychopharmacology and neuroscience : the official scientific journal of the Korean College of Neuropsychopharmacology · 2022
    Article
  9. Article
  10. Protective Role of Glutathione in the Hippocampus after Brain Ischemia.International journal of molecular sciences · 2021
    Review
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  12. Article
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  19. AT1R/GSK-3Oxidative medicine and cellular longevity · 2020
    Article
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

3 authors at 2 institutions in 1 country.

Maha Mohammed Abdel-FattahPharmacology and Toxicology Department, Faculty of Pharmacy, Beni-Suef University, Beni-Suef, Egypt.
Basim Anwar Shehata MessihaPharmacology and Toxicology Department, Faculty of Pharmacy, Beni-Suef University, Beni-Suef, Egypt. drbasimanwar2006@yahoo.com.
Ahmed Mohamed MansourPharmacology and Toxicology Department, Faculty of Pharmacy, Al-Azhar University, Cairo, Egypt.
Beni-Suef University · EGAl-Azhar University · EG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The brain renin-angiotensin system (RAS) is considered a crucial regulator for physiological homeostasis and disease progression. We evaluated the protective effects of the angiotensin receptor blocker (ARB) telmisartan and the angiotensin-converting enzyme 2 (ACE2) activator xanthenone on experimental cerebral ischemia/reperfusion (I/R) injury. Rats were divided into a sham control, a cerebral I/R control, a standard treatment (nimodipine, 10 mg/kg/day, 15 days, p.o.), three telmisartan treatments (1, 3, and 10 mg/kg/day, 15 days, p.o.), and three xanthenone treatments (0.5, 1, and 2 mg/kg/day, 15 days, s.c.) groups. One hour after the last dose, all rats except the sham control group were exposed to 30-min cerebral ischemia followed by 24-h reperfusion. Brain ACE and ACE2 activities and the apoptotic marker caspase-3 levels were assessed. Glutathione (GSH), malondialdehyde (MDA), and nitric oxide end products (NOx) as oxidative markers and tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and IL-10 as immunological markers were assessed. Histopathological examination and immunohistochemical evaluation of glial fibrillary acidic protein (GFAP) were performed in cerebral cortex and hippocampus sections. Telmisartan and xanthenone in the higher doses restored MDA, NOx, TNF-α, IL-6, caspase-3, ACE, and GFAP back to normal levels and significantly increased GSH, IL-10, and ACE2 compared to I/R control values. Histopathologically, both agents showed mild degenerative changes and necrosis of neurons in cerebral cortex and hippocampus compared with I/R control group. Modulation of brain RAS, either through suppression of the classic ACE pathway or stimulation of its antagonist pathway ACE2, may be a promising strategy against cerebral I/R damage.

Indexed as

Angiotensin-Converting Enzyme 2Angiotensin II Type 1 Receptor BlockersAnimalsBrainBrain IschemiaCytokinesGlutathioneMaleMalondialdehydeNitric OxidePeptidyl-Dipeptidase ARats, WistarReperfusion InjuryRNA, MessengerTelmisartanXanthenesAce2 protein, ratAngiotensin-Converting Enzyme 2Angiotensin II Type 1 Receptor BlockersCytokinesGlutathioneMalondialdehydeNitric OxidePeptidyl-Dipeptidase ARNA, MessengerTelmisartanXanthenesACEACE2Ischemia/reperfusionNimodipineTelmisartanXanthenone

Identifiers

PMID29909460
OpenAlexW2808291555

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.