Evidence map›Paper›PMID 31881846›Full record

ArticleBMC neuroscience2019

Lipopolysaccharide worsens the prognosis of experimental cerebral ischemia via interferon gamma-induced protein 10 recruit in the acute stage.

Ping Wang, Jiaqi Zhang, Feifei Guo, Shuang Wang, Yi Zhang, Defeng Li, Haiyu Xu, Hongjun Yang

Open access · goldAbstract read
In one paragraph

Article in BMC neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 2 pooled it
1.0field-weighted citation impact, top 23% 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

13 citing papers in PubMed, 2 syntheses or guidelines pooled it, 18 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. The neurobiological regulatory mechanism of brain edema.Frontiers in cellular neuroscience · 2026
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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.

Ping WangInstitute of Chinese Materia Medica, China Academy of Chinese Medical Sciences, Beijing, 100700, China.
Jiaqi ZhangHeilongjiang University of Chinese Medicine, Harbin, 150040, China.
Feifei GuoInstitute of Chinese Materia Medica, China Academy of Chinese Medical Sciences, Beijing, 100700, China.
Shuang WangHeilongjiang University of Chinese Medicine, Harbin, 150040, China.
Yi ZhangInstitute of Chinese Materia Medica, China Academy of Chinese Medical Sciences, Beijing, 100700, China.
Defeng LiInstitute of Chinese Materia Medica, China Academy of Chinese Medical Sciences, Beijing, 100700, China.
Haiyu XuInstitute of Chinese Materia Medica, China Academy of Chinese Medical Sciences, Beijing, 100700, China. hy_xu627@163.com.ORCID http://orcid.org/0000-0002-6180-864X
Hongjun YangInstitute of Chinese Materia Medica, China Academy of Chinese Medical Sciences, Beijing, 100700, China. hongjun0420@vip.sina.com.
Chinese Academy of Medical Sciences & Peking Union Medical College · CNHeilongjiang University of Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundInfection is an important clinical complication facing stroke-patients and triples the risk of death within 30 days post-stroke via mechanisms which are poorly understood.

aimsWe tried to explore the mechanisms that inflammation caused by infections aggravated the ischemic brain injury after middle cerebral artery occlusion (MCAO).

methodsWe used lipopolysaccharide (LPS) as systemic inflammatory stimuli to explore the mechanisms of aggravated ischemic brain injury after Sprague-Dawley male rats subjected to MCAO. Brain damage was evaluated by cerebral blood perfusion, Longa-5 scores, infarct volume and edema degree. Systemic cytokine responses and inflammatory changes in the plasma and brain were analyzed by ELISA kit, RT

resultsLipopolysaccharide profoundly aggravated the brain damage after 24 h post-MCAO. At the acute stage (ischemia/reperfusion 90 min/3 h), the brain homogenate gene expression of interleukin 6 (IL-6), tumor necrosis factor α (TNF-α), interleukin 1β (IL-1β) and Interferon gamma-induced protein 10 (IP-10) was significantly up-regulated and the contents in plasma and brain homogenate were significantly increased in MCAO and MCAO + LPS group. IP-10 was the only gene with significant difference between MCAO and MCAO + LPS group, which was also in an important position with degrees of ≥ 14 in PPI network.

conclusionsIt was possible that trace LPS aggravated the ischemic brain injury by induction of excessive IP-10 secretion in the acute stage, leading to excessive inflammatory response, which consequently increased the infarct volume and edema degree 24 h post-MCAO.

Indexed as

AnimalsBrainBrain IschemiaCerebrovascular CirculationChemokine CXCL10InflammationInterleukin-1betaInterleukin-6LipopolysaccharidesMalePrognosisRandom AllocationRats, Sprague-DawleyTumor Necrosis Factor-alphaChemokine CXCL10Cxcl10 protein, ratIL1B protein, ratIl6 protein, ratInterleukin-1betaInterleukin-6LipopolysaccharidesTumor Necrosis Factor-alphaCerebral ischemiaInflammationLPSMCAO

Identifiers

PMID31881846
PMCPMC6935231
OpenAlexW2997637189

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LicenceCC BY
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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.