Evidence map›Paper›PMID 32474900›Full record

ArticleJournal of molecular neuroscience : MN2020

Inhibition of IL-32 Expression Ameliorates Cerebral Ischemia-Reperfusion Injury via the NOD/MAPK/NF-κB Signaling Pathway.

Chao Liu, Xiaohui Xu, Chao Huang, Dandan Shang, Li Zhang, Yupeng Wang

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of molecular neuroscience : MN, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.3field-weighted citation impact, top 41% 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

1 citing paper in PubMed, 4 citations in OpenAlex.

  1. 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

6 authors at 1 institution in 1 country.

Chao LiuNeurology Department, Luoyang Central Hospital Affiliated to Zhengzhou University, 288 Zhongzhou Road, Luoyang City, Henan Province, China.
Xiaohui XuNeurology Department, Luoyang Central Hospital Affiliated to Zhengzhou University, 288 Zhongzhou Road, Luoyang City, Henan Province, China. xiaohuixuzz@163.com.
Chao HuangNeurology Department, Luoyang Central Hospital Affiliated to Zhengzhou University, 288 Zhongzhou Road, Luoyang City, Henan Province, China.
Dandan ShangNeurology Department, Luoyang Central Hospital Affiliated to Zhengzhou University, 288 Zhongzhou Road, Luoyang City, Henan Province, China.
Li ZhangNeurology Department, Luoyang Central Hospital Affiliated to Zhengzhou University, 288 Zhongzhou Road, Luoyang City, Henan Province, China.
Yupeng WangNeurology Department, Luoyang Central Hospital Affiliated to Zhengzhou University, 288 Zhongzhou Road, Luoyang City, Henan Province, China.
Luoyang Central Hospital Affiliated to Zhengzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cerebral ischemia represents a major cause of disability, yet its precise mechanism remains unknown. In addition, ischemia-reperfusion injury which occurs during the blood recovery process increases the risk of mortality, and is not adequately addressed with current treatment. To improve therapeutic options, it is important to explore the vital substances that play a pivotal role in ischemia-reperfusion injury. This study is the first to investigate the role of IL-32, a vital pro-inflammatory factor, in models of cerebral ischemia-reperfusion injury. The results showed that IL-32 was highly expressed in both in vivo and in vitro models. The proteins of the NOD/MAPK/NF-κB pathway were also up-regulated, indicating a potential signaling pathway mechanism. Inhibition of IL-32 and blocking of the NOD/MAPK/NF-κB pathway increased cell survival, decreased the level of inflammatory factors and inflammasomes, and attenuated nitrosative stress. Taken together, the results show that inhibition of IL-32 expression ameliorates cerebral ischemia-reperfusion injury via the NOD/MAPK/NF-κB signaling pathway. The findings in this study reveal that IL-32 is a vital target of ischemia-reperfusion injury, providing a new avenue for treatment development.

Indexed as

MAP Kinase Signaling SystemAnimalsAnti-Inflammatory AgentsApoptosisBrainInfarction, Middle Cerebral ArteryInflammasomesInterleukinsMaleNeuroprotective AgentsNF-kappa BNod Signaling Adaptor ProteinsPC12 CellsProtein Kinase InhibitorsRatsRats, Sprague-DawleyAnti-Inflammatory AgentsInflammasomesInterleukinsNeuroprotective AgentsNF-kappa BNod Signaling Adaptor ProteinsProtein Kinase InhibitorsCell apoptosisCell viabilityCerebral ischemia-reperfusion injuryIL-32InflammationNitrosative stressNOD/MAPK/NF-κB signaling pathwayStroke

Identifiers

PMID32474900
OpenAlexW3032193115

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.