Evidence map›Paper›PMID 34055311›Full record

ArticleToxicology research2019

Astilbin attenuates cerebral ischemia/reperfusion injury by inhibiting the TLR4/MyD88/NF-κB pathway.

Jing Li, Zhaowei Gu, Yue Liu, Yu Wang, Min Zhao

RetractedOpen access · bronzeAbstract read
In one paragraph

Article in Toxicology research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.5field-weighted citation impact, top 30% 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

9 citing papers in PubMed, 10 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Jing LiChangchun University of Chinese Medicine , Changchun City , Jilin Province 130000 , China . Email: JingLisdf@163.com ; Tel: +86-0431-81953783.ORCID 0000-0001-5199-1703
Zhaowei GuChangchun University of Chinese Medicine , Changchun City , Jilin Province 130000 , China . Email: JingLisdf@163.com ; Tel: +86-0431-81953783.
Yue LiuChangchun University of Chinese Medicine , Changchun City , Jilin Province 130000 , China . Email: JingLisdf@163.com ; Tel: +86-0431-81953783.
Yu WangChangchun University of Chinese Medicine , Changchun City , Jilin Province 130000 , China . Email: JingLisdf@163.com ; Tel: +86-0431-81953783.
Min ZhaoChangchun University of Chinese Medicine , Changchun City , Jilin Province 130000 , China . Email: JingLisdf@163.com ; Tel: +86-0431-81953783.
Changchun University of Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ischemic stroke is the second most common cause of death worldwide and cerebral ischemia/reperfusion (I/R) injury also leads to serious tissue damage. Astilbin, a natural bioactive flavonoid compound, has been reported to have protective effects on neurological diseases. This study aims to investigate the effects of astilbin on cerebral I/R injury and determine the mechanisms involved. The results demonstrated that, in cerebral I/R rats, astilbin could attenuate I/R injury in the hippocampal region, decreasing the activity of lactate dehydrogenase (LDH) and malondialdehyde (MDA) in the rat brain. Astilbin also inhibited the I/R-induced upregulation of pro-inflammatory mediators (TNFα, IL-1β, IL-6). Similarly, in hypoxia/reperfusion (H/R) treated human neuroblastoma cells, astilbin could increase the cell viability of SH-SY5Y, decrease the activity of LDH and MDA, and inhibit the H/R-induced upregulation of pro-inflammatory mediators. For the mechanism study, western blot results indicated that astilbin could inhibit the expression of Toll-like receptor 4 (TLR4), myeloid differential protein 88 (MYD88) and phosphorylated NF-κB p65 in H/R treated SH-SY5Y cells. The research indicated that astilbin ameliorated cerebral I/R injury partly

Identifiers

PMID34055311
PMCPMC8142934
OpenAlexW2986318119

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.