Evidence map›Paper›PMID 26961544›Full record

ArticleCellular and molecular neurobiology2017

Neuroprotective Effects of Resatorvid Against Traumatic Brain Injury in Rat: Involvement of Neuronal Autophagy and TLR4 Signaling Pathway.

Yan Feng, Junling Gao, Ying Cui, Minghang Li, Ran Li, Changmeng Cui, Jianzhong Cui

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cellular and molecular neurobiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
5.0field-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

40 citing papers in PubMed, 74 citations in OpenAlex.

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  13. Frontiers in neuroscience · 2022
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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

7 authors at 4 institutions in 1 country.

Yan FengDepartment of Surgery, Hebei Medical University, No. 361 East Zhongshan Road, Shijiazhuang, 050017, People's Republic of China.
Junling GaoSchool of Basic Medical Science, North China University of Science and Technology, Tangshan, People's Republic of China.
Ying CuiDepartment of Neurosurgery, Tangshan Workers' Hospital, Tangshan, 063000, Hebei, People's Republic of China.
Minghang LiSchool of Basic Medical Science, North China University of Science and Technology, Tangshan, People's Republic of China.
Ran LiSchool of Basic Medical Science, North China University of Science and Technology, Tangshan, People's Republic of China.
Changmeng CuiDepartment of Surgery, Hebei Medical University, No. 361 East Zhongshan Road, Shijiazhuang, 050017, People's Republic of China.
Jianzhong CuiDepartment of Surgery, Hebei Medical University, No. 361 East Zhongshan Road, Shijiazhuang, 050017, People's Republic of China. jzhcuidr2001@163.com.
North China University of Science and Technology · CNHebei Medical University · CNLiaoning Provincial People's Hospital · CNTangshan People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Accumulating evidence indicates that autophagy and inflammatory responses contributes to secondary brain injury after traumatic brain injury (TBI), and toll-like receptor 4 (TLR4) is considered to involvement of this cascade and plays an important role. The present study was designed to determine the hypothesis that administration of resatorvid (TAK-242), a TLR4 antagonist, might provide a neuroprotective effect by inhibit TLR4-mediated pathway in a TBI rat model. Rat subjected to controlled cortical impact injury were injected with TAK-242 (0.5 mg/kg, i.v. injected) 10 min prior to injury. The results demonstrated that TAK-242 treatment significantly attenuated TBI-induced neurons loss, brain edema, and neurobehavioral impairment in rats. Immunoblotting analysis showed that TAK-242 treatment reduced TBI-induced TLR4, Beclin 1, and LC3-II levels, and maintained p62 levels at 24 h. Double immunolabeling demonstrated that LC3 dots co-localized with the hippocampus pyramidal neurons, and TLR4 was localized with the hippocampus neurons and astrocytes. In addition, the expression of TLR4 downstream signaling molecules, including MyD88, TRIF, NF-κB, TNF-α, and IL-1β, was significantly downregulated in hippocampus tissue by Western blot analysis. In conclusion, our findings indicate that pre-injury treatment with TAK-242 could inhibit neuronal autophagy and neuroinflammation responses in the hippocampus in a rat model of TBI. The neuroprotective effects of TAK-242 may be related to modulation of the TLR4-MyD88/TRIF-NF-κB signaling pathway. Furthermore, the study also suggests that TAK-242, an attractive potential drug, may be a promising drug candidate for TBI.

Indexed as

AnimalsAutophagyBrain Injuries, TraumaticMaleNeuronsNeuroprotective AgentsRandom AllocationRatsRats, Sprague-DawleySignal TransductionSulfonamidesToll-Like Receptor 4Treatment Outcomeethyl 6-(N-(2-chloro-4-fluorophenyl)sulfamoyl)cyclohex-1-ene-1-carboxylateNeuroprotective AgentsSulfonamidesTlr4 protein, ratToll-Like Receptor 4AutophagyNeuroinflammationResatorvid (TAK-242)Toll-like receptor 4 (TLR4)Traumatic brain injury (TBI)

Identifiers

PMID26961544
PMCPMC11482083
OpenAlexW2295605120

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.