Evidence map›Paper›PMID 25644393›Full record

ArticleJournal of neuroinflammation2015

Deferoxamine attenuates lipopolysaccharide-induced neuroinflammation and memory impairment in mice.

Xiao-Ying Zhang, Jiang-Bei Cao, Li-Ming Zhang, Yun-Feng Li, Wei-Dong Mi

Open access · goldAbstract read
In one paragraph

Article in Journal of neuroinflammation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed, 1 pooled it
6.9field-weighted citation impact, top 3% 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

68 citing papers in PubMed, 1 synthesis or guideline pooled it, 138 citations in OpenAlex.

  1. Pooled it
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8 more citing papers are in PubMed but not listed here.

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

5 authors at 2 institutions in 1 country.

Xiao-Ying ZhangAnesthesia and Operation Center, Chinese PLA General Hospital, Beijing, 100853, China. zxystudy@163.com.
Jiang-Bei CaoAnesthesia and Operation Center, Chinese PLA General Hospital, Beijing, 100853, China. cjb2000@sina.com.
Li-Ming ZhangInstitute of Pharmacology and Toxicology, Academy of Military Medical Sciences, Beijing, 100850, China. zhanglm0308@163.com.
Yun-Feng LiInstitute of Pharmacology and Toxicology, Academy of Military Medical Sciences, Beijing, 100850, China. lyf619@aliyun.com.
Wei-Dong MiAnesthesia and Operation Center, Chinese PLA General Hospital, Beijing, 100853, China. mwd1962@sina.cn.
Chinese PLA General Hospital · CNAcademy of Military Medical Sciences · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundNeuroinflammation often results in enduring cognitive impairment and is a risk factor for postoperative cognitive dysfunction. There are currently no effective treatments for infection-induced cognitive impairment. Previous studies have shown that the iron chelator deferoxamine (DFO) can increase the resistance of neurons to injury and disease by stimulating adaptive cellular stress responses. However, the impact of DFO on the cognitive sequelae of neuroinflammation is unknown.

methodsA mouse model of lipopolysaccharide (LPS)-induced cognitive impairment was established to evaluate the neuroprotective effects of DFO against LPS-induced memory deficits and neuroinflammation. Adult C57BL/6 mice were treated with 0.5 μg of DFO 3 days prior to intracerebroventricular microinjection of 2 μg of LPS. Cognitive function was assessed using a Morris water maze from post-injection days 1 to 3. Animal behavioral tests, as well as pathological and biochemical assays were performed to evaluate the LPS-induced hippocampal damage and the neuroprotective effect of DFO.

resultsTreatment of mice with LPS resulted in deficits in cognitive performance in the Morris water maze without changing locomotor activity, which were ameliorated by pretreatment with DFO. DFO prevented LPS-induced microglial activation and elevations of IL-1β and TNF-α levels in the hippocampus. Moreover, DFO attenuated elevated expression of caspase-3, modulated GSK3β activity, and prevented LPS-induced increases of MDA and SOD levels in the hippocampus. DFO also significantly blocked LPS-induced iron accumulation and altered expression of proteins related to iron metabolism in the hippocampus.

conclusionsOur results suggest that DFO may possess a neuroprotective effect against LPS-induced neuroinflammation and cognitive deficits via mechanisms involving maintenance of less brain iron, prevention of neuroinflammation, and alleviation of oxidative stress and apoptosis.

Indexed as

AnimalsCaspase 3DeferoxamineDisease Models, AnimalDose-Response Relationship, DrugEncephalitisExploratory BehaviorGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaInterleukin-1betaIronLipopolysaccharidesMaleMalondialdehydeMaze LearningMemory DisordersCaspase 3DeferoxamineGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaGsk3b protein, mouseInterleukin-1betaIronLipopolysaccharidesMalondialdehydeSiderophoresSuperoxide DismutaseTumor Necrosis Factor-alpha

Identifiers

PMID25644393
PMCPMC4323121
OpenAlexW2168936681

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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.