Evidence map›Paper›PMID 33580874›Full record

ArticleNeurotoxicity research2021

Apelin-36 Protects HT22 Cells Against Oxygen-Glucose Deprivation/Reperfusion-Induced Oxidative Stress and Mitochondrial Dysfunction by Promoting SIRT1-Mediated PINK1/Parkin-Dependent Mitophagy.

Ziqi Shao, Shanshan Dou, Junge Zhu, Huiqing Wang, Dandan Xu, Chunmei Wang, Baohua Cheng, Bo Bai

Abstract read
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Article in Neurotoxicity research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
4.0field-weighted citation impact, top 6% 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

20 citing papers in PubMed, 34 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

8 authors at 3 institutions in 1 country.

Ziqi ShaoCheeloo College of Medicine, Shandong University, Jinan, 250014, China.
Shanshan DouNeurobiology Institute, Jining Medical University, Jining, 272067, China.
Junge ZhuCapital Medical University, Beijing, 100000, China.
Huiqing WangCheeloo College of Medicine, Shandong University, Jinan, 250014, China.
Dandan XuCheeloo College of Medicine, Shandong University, Jinan, 250014, China.
Chunmei WangNeurobiology Institute, Jining Medical University, Jining, 272067, China.
Baohua ChengNeurobiology Institute, Jining Medical University, Jining, 272067, China. chengbh1979@163.com.
Bo BaiNeurobiology Institute, Jining Medical University, Jining, 272067, China.
Jining Medical University · CNShandong University · CNCapital Medical University · CN

Funding

National Natural Science Foundation of China No. 81501018National Natural Science Foundation of China No.81671276National Natural Science Foundation of China No. 81870948Natural Science Foundation of Shandong Province No. ZR2014HL040Program Supporting Foundation for Teachers' Research of Jining Medical University of China No. JYFC2018KJ003
6 · The paper itself

Abstract

Oxidative stress and mitochondrial dysfunction are involved in cerebral ischemia/reperfusion injury-induced neuronal apoptosis. Mitophagy is the main method to eliminate dysfunctional mitochondria. Apelin-36, a type of neuropeptide, has been reported to exert protective effects in cerebral I/R (I/R) injury, but its precise mechanisms remain to be elucidated. To study the effects of Apelin-36 on oxidative stress and mitochondrial dysfunction in cerebral I/R injury, the oxygen-glucose deprivation/reperfusion (OGD/R) model with 6 h of ischemia and 6 h of reperfusion was established in HT22 cells. Results demonstrated that Apelin-36 protected against OGD/R injury by improving cell viability, decreasing the apoptotic cells ratio and increasing the ratio of Bcl-2/Bax. In addition, Apelin-36 treatment inhibited oxidative stress by downregulating the level of reactive oxygen species (ROS) and malondialdehyde (MDA) as well as the expression of inducible nitric oxide synthase (iNOS). And Apelin-36 also activated the level of superoxide dismutase (SOD) and glutathione (GSH). Mitochondrial apoptosis was also alleviated with Apelin-36 treatment detected by the mitochondrial membrane potential (MMP) and the expression of Cytochrome c (Cyt c), Cleaved caspase-9, and Cleaved caspase-3. Furthermore, the SIRT1-mediated PINK1/Parkin-dependent mitophagy was activated by Apelin-36 treatment with the downregulation of p62 and upregulation of LC3B-II and Beclin1. Both EX527 and Cyclosporine A (CsA), which are inhibitors of SIRT1 and mitophagy, markedly alleviated the inhibition of oxidative stress and mitochondrial dysfunction caused by Apelin-36. These findings suggest that SIRT1-mediated PINK1/Parkin-dependent mitophagy is involved in the neuroprotective effects of Apelin-36 on OGD/R-induced oxidative stress and mitochondrial dysfunction.

Indexed as

AnimalsApelinCell HypoxiaCell Line, TransformedGlucoseMembrane Potential, MitochondrialMiceMitochondriaMitophagyNeuroprotective AgentsOxidative StressProtein KinasesPTEN-Induced Putative KinaseReactive Oxygen SpeciesSirtuin 1Ubiquitin-Protein LigasesApelinApln protein, mouseGlucoseNeuroprotective Agentsparkin proteinProtein KinasesPTEN-Induced Putative KinaseReactive Oxygen SpeciesSirt1 protein, mouseSirtuin 1Ubiquitin-Protein LigasesApelin-36Mitochondrial dysfunctionMitophagyOxidative stressOxygen-glucose deprivation/reperfusion injury

Identifiers

PMID33580874
OpenAlexW3126966499

What OpenQuestion holds

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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.