Evidence map›Paper›PMID 26429193›Full record

ArticleCellular and molecular neurobiology2016

Protective Effects of UCF-101 on Cerebral Ischemia-Reperfusion (CIR) is Depended on the MAPK/p38/ERK Signaling Pathway.

Danying Su, Jing Ma, Zhuobo Zhang, Ye Tian, Baozhong Shen

Open access · greenAbstract read
In one paragraph

Article in Cellular and molecular neurobiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.9field-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

11 citing papers in PubMed, 15 citations in OpenAlex.

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  6. Mechanism of Progesterone in Treatment of Traumatic Brain Injury Based on Network Pharmacology and Molecular Docking Technology.Medical science monitor : international medical journal of experimental and clinical research · 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

5 authors at 2 institutions in 1 country.

Danying SuDepartment of Neurology, The Fourth Affiliated Hospital of Harbin Medical University, 150000, Harbin, People's Republic of China.
Jing MaDepartment of Anatomy, Harbin Medical University, 150000, Harbin, People's Republic of China. Jingma2009@aliyun.com.
Zhuobo ZhangDepartment of Neurology, The Fourth Affiliated Hospital of Harbin Medical University, 150000, Harbin, People's Republic of China.
Ye TianDepartment of Cardiology, The First Affiliated Hospital of Harbin Medical University, 150000, Harbin, People's Republic of China.
Baozhong ShenDepartment of Imaging, The Fourth Affiliated Hospital Harbin Medical University, No. 37 Yiyuan Str, Nangang District, 150001, Harbin, People's Republic of China. baozhong_shen@163.com.
Harbin Medical University · CNFourth Affiliated Hospital of Harbin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

This study was aimed to investigate the treatment mechanisms of 5-[5-(2-nitrophenyl) furfuryliodine]-1,3-diphenyl-2-thiobarbituric acid (UCF-101) in cerebral ischemia-reperfusion (CIR) model rats. Total of 54 healthy male Wistar rats were randomly assigned into three groups, namely sham group, vehicle group, and UCF-101 group. The CIR-injured model was established by right middle cerebral artery occlusion and reperfusion. Neurological function was assessed by an investigator according to the Longa neurologic deficit scores. Meanwhile, the cerebral tissue morphology and apoptotic neurons were evaluated by H&E and TUNEL staining, respectively. Additionally, the expressions of caspase 3, p-p38, and p-ERK were detected by immunohistochemistry or/and Western blotting assays. As results, neurologic deficit and pathological damage were obviously enhanced and TUNEL positive neurons were significantly increased in CIR-injured rats, as compared with those in sham group. Furthermore, the expressions of caspase 3, p-p38, and p-ERK were also significantly increased in vehicle group than those in sham group (P < 0.05). However, UCF-101 treatment could markedly weaken the neurologic deficit with lower scores and improve pathological condition. After UCF-101 treatment, TUNEL positive neurons as well as the expression of caspase 3 were significantly decreased than those in vehicle group (P < 0.05). Besides, p-p38 was decreased while p-ERK was increased in UCF-101 group than those in vehicle group (P < 0.05). Therefore, we concluded that the protective effects of UCF-101 might be associated with apoptosis process and MAPK signaling pathway in the CIR-injured model.

Indexed as

AnimalsApoptosisBrain IschemiaDisease Models, AnimalInfarction, Middle Cerebral ArteryMaleMAP Kinase Signaling SystemPyrimidinonesRats, WistarReperfusion InjuryThionesPyrimidinonesThionesUCF 101Apoptosis neuronsCerebral ischemia–reperfusionMAPKUCF-101

Identifiers

PMID26429193
PMCPMC11482449
OpenAlexW1851705678

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.