Evidence map›Paper›PMID 28488233›Full record

ArticleNeurochemical research2017

P2X7 Participates in Intracerebral Hemorrhage-Induced Secondary Brain Injury in Rats via MAPKs Signaling Pathways.

Zunjia Wen, Binbin Mei, Haiying Li, Yang Dou, Xiaodi Tian, Meifen Shen, Gang Chen

Abstract read
PubMed Publisher
In one paragraph

Article in Neurochemical research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

18 citing papers in PubMed, 31 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

7 authors at 2 institutions in 1 country.

Zunjia WenDepartment of Neurosurgery and Brain and Nerve Research Laboratory, The First Affiliated Hospital of Soochow University, 188 Shizi Street, Suzhou, 215006, China.
Binbin MeiDepartment of Neurosurgery and Brain and Nerve Research Laboratory, The First Affiliated Hospital of Soochow University, 188 Shizi Street, Suzhou, 215006, China.
Haiying LiDepartment of Neurosurgery and Brain and Nerve Research Laboratory, The First Affiliated Hospital of Soochow University, 188 Shizi Street, Suzhou, 215006, China.
Yang DouDepartment of Neurosurgery and Brain and Nerve Research Laboratory, The First Affiliated Hospital of Soochow University, 188 Shizi Street, Suzhou, 215006, China.
Xiaodi TianDepartment of Neurosurgery and Brain and Nerve Research Laboratory, The First Affiliated Hospital of Soochow University, 188 Shizi Street, Suzhou, 215006, China.
Meifen ShenDepartment of Neurosurgery and Brain and Nerve Research Laboratory, The First Affiliated Hospital of Soochow University, 188 Shizi Street, Suzhou, 215006, China. sz_meifenshen@sina.com.
Gang ChenDepartment of Neurosurgery and Brain and Nerve Research Laboratory, The First Affiliated Hospital of Soochow University, 188 Shizi Street, Suzhou, 215006, China. nju_neurosurgery@163.com.
First Affiliated Hospital of Soochow University · CNSoochow University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

This study aimed to study the role of P2X7 in intracerebral hemorrhage (ICH)-induced secondary brain injury (SBI) and the underlying mechanisms. An autologous blood injection was used to induce ICH model in Sprague-Dawley rats, and cultured primary rat cortical neurons were exposed to oxyhemoglobin to mimic ICH in vitro. siRNA interference and over-expression of P2X7, agonists and antagonists of P2X7, p38 MAPK and ERK were exploited. The protein levels were assessed using Western blotting and immunofluorescence staining. Terminal deoxynucleotidyl transferase dUTP nick end labeling staining and Fluoro-Jade B were conducted to detect apoptotic and degenerating neurons. The protein levels of P2X7, phosphorylated p38, ERK, active caspase-3 and NF-κB were significantly increased by ICH, which could be further increased by BzATP (P2X7 agonist) and reduced by BBG (P2X7 antagonist). And BzATP demonstrated a significant increase in cell death ratio and brain water content, while BBG led to a reverse results. In addition, Over- P2X7 increased the levels of P2X7, phosphorylated p38, ERK, active caspase-3 and NF-κB, and aggravated cell apoptosis, while si P2X7 resulted in opposite effects. Finally, the protein levels of phosphorylated P38 and active caspase 3 were decreased by BzATP plus Hydrochloride (p38 MAPK antagonist) and increased vy BBG plus Asiatic acid (p38 MAPK agonist), while the protein levels of phosphorylated ERK and NF-κB were decreased with BzATP plus Nimbolide (ERK antagonist) and increased with BBG plus Saikosaponin C (ERK agonist). This study demonstrates that inhibition of P2X7 could prevent ICH-induced SBI via MAPKs signaling pathway.

Indexed as

AnimalsBrain InjuriesCells, CulturedCerebral HemorrhageMaleMAP Kinase Signaling SystemPurinergic P2X Receptor AntagonistsRandom AllocationRatsRats, Sprague-DawleyReceptors, Purinergic P2X7Purinergic P2X Receptor AntagonistsReceptors, Purinergic P2X7Intracerebral hemorrhageMAPKsP2X7Secondary brain injury

Identifiers

PMID28488233
OpenAlexW2613009520

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.