Evidence map›Paper›PMID 27180190›Full record

ArticleNeurochemical research2016

Protective Effect of Aliskiren in Experimental Ischemic Stroke: Up-Regulated p-PI3K, p-AKT, Bcl-2 Expression, Attenuated Bax Expression.

Jiangyong Miao, Lina Wang, Xiangjian Zhang, Chunhua Zhu, Lili Cui, Hui Ji, Ying Liu, Xiaolu Wang

Abstract read
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In one paragraph

Article in Neurochemical research, 2016. 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
3.4field-weighted citation impact, top 7% 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.

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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

8 authors at 2 institutions in 1 country.

Jiangyong MiaoDepartment of Neurology, Second Hospital of Hebei Medical University, Shijiazhuang, 050000, Hebei, People's Republic of China.
Lina WangDepartment of Neurology, Second Hospital of Hebei Medical University, Shijiazhuang, 050000, Hebei, People's Republic of China.
Xiangjian ZhangDepartment of Neurology, Second Hospital of Hebei Medical University, Shijiazhuang, 050000, Hebei, People's Republic of China. zhang6xj@aliyun.com.
Chunhua ZhuDepartment of Neurology, Second Hospital of Hebei Medical University, Shijiazhuang, 050000, Hebei, People's Republic of China.
Lili CuiDepartment of Neurology, Second Hospital of Hebei Medical University, Shijiazhuang, 050000, Hebei, People's Republic of China.
Hui JiDepartment of Neurology, Second Hospital of Hebei Medical University, Shijiazhuang, 050000, Hebei, People's Republic of China.
Ying LiuDepartment of Neurology, Second Hospital of Hebei Medical University, Shijiazhuang, 050000, Hebei, People's Republic of China.
Xiaolu WangHebei Collaborative Innovation Center for Cardio-cerebrovascular Disease, Shijiazhuang, 050000, Hebei, People's Republic of China. wangxl2014@yahoo.com.
Second Hospital of Hebei Medical University · CNHebei Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aliskiren (ALK), a pharmacological renin inhibitor, is an effective antihypertensive drug and has potent anti-apoptotic activity, but it is currently unknown whether ALK is able to attenuate brain damage caused by acute cerebral ischemia independent of its blood pressure-lowering effects. This study aimed to investigate the role of ALK and its potential mechanism in cerebral ischemia. C57/BL6 mice were subjected to transient middle cerebral artery occlusion (tMCAO) and treated for 5 days with Vehicle or ALK (10 or 25 mg/kg per day via intragastric administration), whereas Sham-operated animals served as controls. Treatment with ALK significantly improved neurological deficits, infarct volume, brain water content and Nissl bodies after stroke (P < 0.05), which did not affect systemic blood pressure. Furthermore, the protection of ALK was also related to decreased levels of apoptosis in mice by enhanced activation of phosphatidylinositol 3-kinase (PI3K)/AKT pathway, increased level of Bcl-2 and reduced Bax expression (P < 0.05). In addition, ALK's effects were reversed by PI3K inhibitors LY294002 (P < 0.05). Our data indicated that ALK protected the brain from reperfusion injuries without affecting blood pressure, and this effect may be through PI3K/AKT signaling pathway.

Indexed as

AmidesAnimalsApoptosisbcl-2-Associated X ProteinBrain IschemiaFumaratesMaleMice, Inbred C57BLNeuroprotective AgentsPhosphatidylinositol 3-KinaseProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-bcl-2Signal TransductionStrokeUp-RegulationaliskirenAmidesBax protein, mousebcl-2-Associated X ProteinFumaratesNeuroprotective AgentsPhosphatidylinositol 3-KinaseProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-bcl-2AliskirenApoptosisCerebral ischemiaNeuroprotection

Identifiers

PMID27180190
OpenAlexW2369126497

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.