Evidence map›Paper›PMID 35037165›Full record

ArticleNeurochemical research2022

Curcumin Attenuates the PERK-eIF2α Signaling to Relieve Acrylamide-Induced Neurotoxicity in SH‑SY5Y Neuroblastoma Cells.

Dandan Yan, Na Wang, Jianling Yao, Xu Wu, Jingping Yuan, Hong Yan

Abstract read
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In one paragraph

Article in Neurochemical research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
2.1field-weighted citation impact, top 15% 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

7 citing papers in PubMed, 14 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

6 authors at 2 institutions in 1 country.

Dandan YanDepartment of Pathology, Renmin Hospital of Wuhan University, 238 Jiefang-Road, Wuchang District, Wuhan, 430060, China.
Na WangDepartment of Health Toxicology, MOE Key Lab of Environment and Health, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, 13 Hangkong-Road, Wuhan, 430030, China.
Jianling YaoDepartment of Health Toxicology, MOE Key Lab of Environment and Health, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, 13 Hangkong-Road, Wuhan, 430030, China.
Xu WuDepartment of Health Toxicology, MOE Key Lab of Environment and Health, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, 13 Hangkong-Road, Wuhan, 430030, China.
Jingping YuanDepartment of Pathology, Renmin Hospital of Wuhan University, 238 Jiefang-Road, Wuchang District, Wuhan, 430060, China. yuanjingping@whu.edu.cn.ORCID http://orcid.org/0000-0002-9213-1096
Hong YanDepartment of Health Toxicology, MOE Key Lab of Environment and Health, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, 13 Hangkong-Road, Wuhan, 430030, China. yanhong@mails.tjmu.edu.cn.
Huazhong University of Science and Technology · CNWuhan University · CN

Funding

National Natural Science Foundation of China 81973092National Natural Science Foundation of China 82003490
6 · The paper itself

Abstract

Curcumin is a natural polyphenolic compound with neuroprotective and antioxidant properties. Acrylamide (ACR) is a by-product of food processing that produces neurotoxicity in humans and animals. The pancreatic endoplasmic reticulum kinase (PERK)-eukaryotic initiation factor-2α (eIF2α) signaling is involved in the occurrence of neurotoxicities. This study is aimed to investigate the protective effect of curcumin on ACR-induced cytotoxicity and explore the role of PERK-eIF2α signaling in this process. ACR exposure at 2.5 mM for 24 h caused oxidative stress as revealed by the distinct increase in cellular reactive oxygen species (ROS) and malondialdehyde (MDA) level, and a significant decrease in glutathione (GSH) content. ACR induced phosphorylated tau aggregation, phosphorylated cAMP response elements binding protein (CREB) reduction, and Bax/Bcl-2 ratio up-regulation in SH-SY5Y cells. ACR also activated the PERK-eIF2α signaling in SH-SY5Y cells and triggered the activation of glycogen synthase kinase-3β (GSK-3β), up-regulated activating transcription factor 4 (ATF4) and C/EBP homologous protein (CHOP). Curcumin pretreatment significantly attenuated ACR-induced neuronal toxicity as revealed by the ameliorated cell viability, mitigated intracellular ROS and MDA level, and elevated GSH content. Moreover, curcumin pretreatment inhibited PERK-dependent eIF2α phosphorylation, further suppressed GSK-3β and ATF4 function, and abolished abnormal tau phosphorylation, P-CREB reduction, and CHOP-induced apoptosis in SH-SY5Y cells. These results provided empirical evidence between curcumin and PERK-eIF2α signaling in ACR-induced neurotoxicity.

Indexed as

CurcumineIF-2 KinaseEukaryotic Initiation Factor-2NeuroblastomaAcrylamideAnimalsApoptosisCell Line, TumorGlycogen Synthase Kinase 3 betaHumansOxidative StressAcrylamideCurcuminEIF2AK3 protein, humaneIF-2 KinaseEukaryotic Initiation Factor-2Glycogen Synthase Kinase 3 betaAcrylamideApoptosisCurcuminOxidative stressPERK-eIF2α signalingTau phosphorylation

Identifiers

PMID35037165
OpenAlexW4205836596

What OpenQuestion holds

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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.