Evidence map›Paper›PMID 27255374›Full record

ArticleInflammation2016

Salvianolic Acid B Ameliorates Cerebral Ischemia/Reperfusion Injury Through Inhibiting TLR4/MyD88 Signaling Pathway.

Yujue Wang, Guang Chen, Xiangdong Yu, Yunchao Li, Li Zhang, Zongze He, Nannan Zhang, Xiuping Yang, Yansheng Zhao, Na Li and 1 more

Abstract read
PubMed Publisher
In one paragraph

Article in Inflammation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
5.3field-weighted citation impact, top 4% 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

33 citing papers in PubMed, 99 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

11 authors at 4 institutions in 1 country.

Yujue WangDepartment of Neurosurgery, KaiLuan General Hospital, Tangshan, 063000, China.
Guang ChenDepartment of Neurosurgery, KaiLuan General Hospital, Tangshan, 063000, China.
Xiangdong YuDepartment of Neurosurgery, KaiLuan General Hospital, Tangshan, 063000, China.
Yunchao LiDepartment of Neurosurgery, KaiLuan General Hospital, Tangshan, 063000, China.
Li ZhangDepartment of Neurosurgery, Tangshan People's Hospital, Tangshan, 063000, China.
Zongze HeDepartment of Neurosurgery, The Affiliated Hospital of University of Electronic Science and Technology of China & Sichuan Provincial People's Hospital, Chengdu, 610072, China.
Nannan ZhangDepartment of Neurology, KaiLuan General Hospital, Tangshan, 063000, China.
Xiuping YangDepartment of Neurology, KaiLuan General Hospital, Tangshan, 063000, China.
Yansheng ZhaoDepartment of Nuclear Magnetic, KaiLuan General Hospital, Tangshan, 063000, China.
Na LiDepartment of Emergency, Chinese People's Liberation Army 255 Hospital, Tangshan, 063000, China.
Hong QiuDepartment of Neurosurgery, KaiLuan General Hospital, Tangshan, 063000, China. shenjingwaikekl@sina.com.
Kailuan General Hospital · CNChinese People's Liberation Army · CNTangshan People's Hospital · CNUniversity of Electronic Science and Technology of China · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ischemic stroke can activate multiple transcription factors and cause inflammatory reactions, which involve pattern recognition receptors with immunostimulatory effects. Toll-like receptor 4 (TLR4) is one of the receptors related to innate immunity and several inflammatory reactions. The promising anti- inflammatory activity of salvianolic acid B (SAB) had been previously reported, but its effect on ischemic stroke remains unknown. An oxygen-glucose deprivation and reoxygenation (OGD/R) model in vitro and a middle cerebral artery occlusion (MCAO) model in vivo were used in this paper, and the results showned that SAB remarkably increased the viabilities of PC12 cells and primary cortical neurons after OGD/R injury and notably prevented cerebral ischemia/reperfusion (I/R) injury. SAB also significantly ameliorated NeuN release from primary cortical neurons. Further research indicated that the neuroprotection of SAB was completed through inhibiting the TLR4/MyD88/TRAF6 signaling pathway. The blocking of TLR4 by SAB also restrained NF-kB transcriptional activity and pro-inflammatory cytokine responses (IL-1β, IL-6, and TNF-α). These findings supply a new insight that will aid in clarifying the effect of SAB against cerebral I/R injury and provide the development of SAB as a potential candidate for treating ischemic stroke.

Indexed as

AnimalsAnti-Inflammatory AgentsBenzofuransBrain IschemiaCells, CulturedCytokinesDepsidesDisease Models, AnimalInfarction, Middle Cerebral ArteryMyeloid Differentiation Factor 88NeuronsNeuroprotective AgentsPC12 CellsRatsReperfusion InjurySignal TransductionAnti-Inflammatory AgentsBenzofuransCytokinesDepsidesMyd88 protein, ratMyeloid Differentiation Factor 88Neuroprotective Agentssalvianolic acid BTLR4 protein, humanTNF Receptor-Associated Factor 6Toll-Like Receptor 4cerebral I/R injuryinflammationischemic strokeSABTLR4

Identifiers

PMID27255374
OpenAlexW2470979441

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.