Evidence map›Paper›PMID 35821335›Full record

ArticleNeuroscience bulletin2022

Anti-Seizure and Neuronal Protective Effects of Irisin in Kainic Acid-Induced Chronic Epilepsy Model with Spontaneous Seizures.

Jie Yu, Yao Cheng, Yaru Cui, Yujie Zhai, Wenshen Zhang, Mengdi Zhang, Wenyu Xin, Jia Liang, Xiaohong Pan, Qiaoyun Wang and 1 more

Open access · greenAbstract read
In one paragraph

Article in Neuroscience bulletin, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

8 citing papers in PubMed, 15 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 3 institutions in 1 country.

Jie Yu *School of Pharmaceutical Sciences, Binzhou Medical University, Yantai, 264003, China.
Yao Cheng *School of Pharmaceutical Sciences, Binzhou Medical University, Yantai, 264003, China.
Yaru Cui *School of Pharmaceutical Sciences, Binzhou Medical University, Yantai, 264003, China.
Yujie ZhaiSchool of Pharmaceutical Sciences, Binzhou Medical University, Yantai, 264003, China.
Wenshen ZhangThe Sixth Scientific Research Department, Shandong Institute of Nonmetallic Materials, Jinan, 250031, China.
Mengdi ZhangSchool of Pharmaceutical Sciences, Binzhou Medical University, Yantai, 264003, China.
Wenyu XinSchool of Pharmaceutical Sciences, Binzhou Medical University, Yantai, 264003, China.
Jia LiangSchool of Pharmaceutical Sciences, Binzhou Medical University, Yantai, 264003, China.
Xiaohong PanSchool of Pharmaceutical Sciences, Binzhou Medical University, Yantai, 264003, China.
Qiaoyun WangSchool of Pharmaceutical Sciences, Binzhou Medical University, Yantai, 264003, China. byylwqy@163.com.
Hongliu SunSchool of Pharmaceutical Sciences, Binzhou Medical University, Yantai, 264003, China. sun_china6@163.com.
Binzhou University · CNBinzhou Medical University · CNShandong Institute of Metrology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

An increased level of reactive oxygen species is a key factor in neuronal apoptosis and epileptic seizures. Irisin reportedly attenuates the apoptosis and injury induced by oxidative stress. Therefore, we evaluated the effects of exogenous irisin in a kainic acid (KA)-induced chronic spontaneous epilepsy rat model. The results indicated that exogenous irisin significantly attenuated the KA-induced neuronal injury, learning and memory defects, and seizures. Irisin treatment also increased the levels of brain-derived neurotrophic factor (BDNF) and uncoupling protein 2 (UCP2), which were initially reduced following KA administration. Furthermore, the specific inhibitor of UCP2 (genipin) was administered to evaluate the possible protective mechanism of irisin. The reduced apoptosis, neurodegeneration, and spontaneous seizures in rats treated with irisin were significantly reversed by genipin administration. Our findings indicated that neuronal injury in KA-induced chronic epilepsy might be related to reduced levels of BDNF and UCP2. Moreover, our results confirmed the inhibition of neuronal injury and epileptic seizures by exogenous irisin. The protective effects of irisin may be mediated through the BDNF-mediated UCP2 level. Our results thus highlight irisin as a valuable therapeutic strategy against neuronal injury and epileptic seizures.

Indexed as

EpilepsyKainic AcidAnimalsBrain-Derived Neurotrophic FactorFibronectinsHippocampusIridoidsRatsRats, Sprague-DawleySeizuresBrain-Derived Neurotrophic FactorFibronectinsgenipinIridoidsKainic AcidEpilepsyGenipinIrisinNeuronal injurySeizure

Identifiers

PMID35821335
PMCPMC9672298
OpenAlexW4285092717

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.