Evidence map›Paper›PMID 26730961›Full record

ArticlePloS one2016

Neuroprotective Effect of Scutellarin on Ischemic Cerebral Injury by Down-Regulating the Expression of Angiotensin-Converting Enzyme and AT1 Receptor.

Wenjuan Wang, Xiaotang Ma, Jichun Han, Mingjie Zhou, Huanhuan Ren, Qunwen Pan, Chunli Zheng, Qiusheng Zheng

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
3.5field-weighted citation impact, top 8% 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

35 citing papers in PubMed, 73 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 6 institutions in 1 country.

Wenjuan WangPharmacy School, Shihezi University, Shihezi, China.
Xiaotang MaInstitute of Neurological Disease, Zhanjiang Medical College, Zhanjiang, Guangdong, China.
Jichun HanPharmacy School, Shihezi University, Shihezi, China.
Mingjie ZhouWeifang Medical University, Weifang, China.
Huanhuan RenPharmacy School, Shihezi University, Shihezi, China.
Qunwen PanInstitute of Neurological Disease, Zhanjiang Medical College, Zhanjiang, Guangdong, China.
Chunli ZhengCollege of Life Sciences, Northwest A&F University, Yangling, Shanxi, China.
Qiusheng ZhengPharmacy School, Shihezi University, Shihezi, China.
Guangdong Medical College · CNShihezi University · CNBinzhou Medical University · CNNorthwest A&F University · CNWeifang Medical University · CNXinjiang Production and Construction Corps · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

background and purposePrevious studies have demonstrated that angiotensin-converting enzyme (ACE) is involved in brain ischemic injury. In the present study, we investigated whether Scutellarin (Scu) exerts neuroprotective effects by down-regulating the Expression of Angiotensin-Converting Enzyme and AT1 receptor in a rat model of permanent focal cerebral ischemia.

methodsAdult Sprague-Dawley rats were administrated with different dosages of Scu by oral gavage for 7 days and underwent permanent middle cerebral artery occlusion (pMCAO). Blood pressure was measured 7 days after Scu administration and 24 h after pMCAO surgery by using a noninvasive tail cuff method. Cerebral blood flow (CBF) was determined by Laser Doppler perfusion monitor and the neuronal dysfunction was evaluated by analysis of neurological deficits before being sacrificed at 24 h after pMCAO. Histopathological change, cell apoptosis and infarct area were respectively determined by hematoxylin-eosin staining, terminal deoxynucleotidyl transfer-mediated dUTP nick end labeling (TUNEL) analysis and 2,3,5-triphenyltetrazolium chloride staining. Tissue angiotensin II (Ang II) and ACE activity were detected by enzyme-linked immunosorbent assays. The expression levels of ACE, Ang II type 1 receptor (AT1R), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin-1β (IL-1β) were measured by Western blot and real-time PCR. ACE inhibitory activity of Scu in vitro was detected by the photometric determination.

resultsScu treatment dose-dependently decreased neurological deficit score, infarct area, cell apoptosis and morphological changes induced by pMCAO, which were associated with reductions of ACE and AT1R expression and the levels of Ang II, TNF-α, IL-6, and IL-1β in ischemic brains. Scu has a potent ACE inhibiting activity.

conclusionScu protects brain from acute ischemic injury probably through its inhibitory effect on the ACE/Ang II/AT1 axis, CBF preservation and proinflammation inhibition.

Indexed as

AnimalsApigeninBrainBrain IschemiaDisease Models, AnimalDown-RegulationGlucuronatesInfarction, Middle Cerebral ArteryInterleukin-1betaInterleukin-6Neuroprotective AgentsPeptidyl-Dipeptidase ARatsRats, Sprague-DawleyReceptor, Angiotensin, Type 1Tumor Necrosis Factor-alphaApigeninGlucuronatesInterleukin-1betaInterleukin-6Neuroprotective AgentsPeptidyl-Dipeptidase AReceptor, Angiotensin, Type 1scutellarinTumor Necrosis Factor-alpha

Identifiers

PMID26730961
PMCPMC4711585
OpenAlexW2224210250

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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.