Evidence map›Paper›PMID 28868122›Full record

ArticleIranian journal of basic medical sciences2017

Allicin attenuates tunicamycin-induced cognitive deficits in rats via its synaptic plasticity regulatory activity.

Qiong Xiang, Xian-Hui Li, Bo Yang, Xin-Xing Fang, Jing Jia, Jie Ren, Yu-Chun Dong, Cheng Ou-Yang, Guang-Cheng Wang

Open access · greenAbstract read
In one paragraph

Article in Iranian journal of basic medical sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.5field-weighted citation impact, top 12% 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

5 citing papers in PubMed, 7 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Article
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

9 authors at 1 institution in 1 country.

Qiong XiangInstitute of Medicine, Medical Research Center, Jishou University, Hunan, China.
Xian-Hui LiInstitute of Medicine, Medical Research Center, Jishou University, Hunan, China.
Bo YangJishou University First Affiliated Hospital, Jishou University, Hunan, China.
Xin-Xing FangInstitute of Medicine, Medical Research Center, Jishou University, Hunan, China.
Jing JiaInstitute of Medicine, Medical Research Center, Jishou University, Hunan, China.
Jie RenInstitute of Medicine, Medical Research Center, Jishou University, Hunan, China.
Yu-Chun DongInstitute of Medicine, Medical Research Center, Jishou University, Hunan, China.
Cheng Ou-YangInstitute of Medicine, Medical Research Center, Jishou University, Hunan, China.
Guang-Cheng WangCollege of Chemistry and Chemical Engineering, Jishou University, Hunan, China.
Jishou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesTo illuminate the functional effects of allicin on rats with cognitive deficits induced by tunicamycin (TM) and the molecular mechanism of this process. MATERIALS AND

methods200-250 g male SD rats were divided into three groups at random: control group (n=12), TM group (5 μl, 50 μM, ICV, n=12), and allicin treatment group (180 mg/kg/d with chow diet, n=12). After 16 weeks of allicin treatment, the learning ability and memory were tested using novel object recognition (NOR) testing on rats with 72 hr TM treatment (5 μl, 50 μM, ICV); meanwhile, the variation of field excitatory postsynaptic potential (fEPSP) in the Schaffer Collateral (SC)-CA1 synapse was detected by extracellular electrophysiological recordings and the morphology of dendritic spine was observed by Golgi staining as well as detecting several synaptic plasticity-related proteins by Western blot.

resultsThe density of dendritic spine was increased significantly in allicin-treated groups and the correspondence slope of fEPSP in TM-induced cognitive deficits group was enhanced and expression of synaptophysin and glutamate receptor-1(GluR1) in hippocampal neurons was up-regulated.

conclusionThe results indicate that allicin plays an important role in synaptic plasticity regulation. These finding showed that allicin could be used as a pharmacologic treatment in TM-induced cognitive deficits.

Indexed as

AllicinDendritic spine densityfEPSPHippocampusSynaptic plasticity

Identifiers

PMID28868122
PMCPMC5569445
OpenAlexW2621205194

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.