Evidence map›Paper›PMID 30382449›Full record

ArticleNeurochemical research2018

Nrf2 Signaling Elicits a Neuroprotective Role Against PFOS-mediated Oxidative Damage and Apoptosis.

Pingping Sun, Xiaoke Nie, Xiaoxu Chen, Lifeng Yin, Jiashan Luo, Lingli Sun, Chunhua Wan, Shengyang Jiang

Abstract read
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In one paragraph

Article in Neurochemical research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
–field-weighted citation impact
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

18 citing papers in PubMed.

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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.

Pingping SunDepartment of Occupational Medicine and Environmental Toxicology, School of Public Health, Nantong University, Nantong, Jiangsu, People's Republic of China.
Xiaoke NieXinglin College, Nantong University, Nantong, Jiangsu, People's Republic of China.
Xiaoxu ChenDepartment of Occupational Medicine and Environmental Toxicology, School of Public Health, Nantong University, Nantong, Jiangsu, People's Republic of China.
Lifeng YinDepartment of Occupational Medicine and Environmental Toxicology, School of Public Health, Nantong University, Nantong, Jiangsu, People's Republic of China.
Jiashan LuoDepartment of Occupational Medicine and Environmental Toxicology, School of Public Health, Nantong University, Nantong, Jiangsu, People's Republic of China.
Lingli SunDepartment of Nutrition and Food Hygiene, School of Public Health, Nantong University, Nantong, Jiangsu, People's Republic of China.
Chunhua WanDepartment of Nutrition and Food Hygiene, School of Public Health, Nantong University, Nantong, Jiangsu, People's Republic of China. chwan@ntu.edu.cn.
Shengyang JiangDepartment of Occupational Medicine and Environmental Toxicology, School of Public Health, Nantong University, 226019, Nantong, Jiangsu, People's Republic of China. jiang_shengyang@163.com.ORCID http://orcid.org/0000-0003-2996-3428

Funding

National Natural Science Foundation of China 81573188
6 · The paper itself

Abstract

Perfluorooctanesulfonate (PFOS) may cause neurotoxicity through the initiation of oxidative stress. In the current study, we investigated the role of anti-oxidant nuclear factor erythroid 2-related factor 2 (Nrf2) pathway in PFOS-induced neurotoxicity. We found that human neuroblastoma SH-SY5Y cells exhibited significant apoptotic cell death following PFOS exposure, and this process was accompanied with apparent accumulation of reactive oxidative species (ROS). In addition, we revealed that PFOS exposure caused marked activation of Nrf2 pathway and the expression of Nrf2 transcription target heme oxygenase-1. We further found that pre-treatment with ROS scavenger N-acetyl-L-cysteine (NAC) dramatically ameliorated PFOS-induced ROS production and Nrf2 signaling. In keeping with these findings, western blot and Cell Counter Kit-8 analyses revealed that pre-incubation with NAC suppressed PFOS-induced expression of pro-apoptotic proteins and impairment of neuronal viability. Moreover, antagonizing Nrf2 pathway with Nrf2 inhibitor brusatol resulted in increased ROS production and enhanced PFOS-induced expression of apoptosis related proteins. Finally, we showed that PFOS exposure altered mitochondrial transmembrane potential and disrupted normal mitochondrial morphology in SH-SY5Y cells. Whereas treatment with NAC ameliorated PFOS-induced mitochondrial disorders, co-incubation with brusatol augmented PFOS-induced mitochondrial deficits, consequently contributing to neuronal apoptosis. These results manifest that Nrf2 pathway plays a protective role in PFOS-induced neurotoxicity, providing new insights into the prevention and treatment of PFOS-related toxicities.

Indexed as

Alkanesulfonic AcidsApoptosisCell Line, TumorDose-Response Relationship, DrugFluorocarbonsHumansNeuroprotectionNF-E2-Related Factor 2Oxidative StressSignal TransductionAlkanesulfonic AcidsFluorocarbonsNFE2L2 protein, humanNF-E2-Related Factor 2perfluorooctane sulfonic acidApoptosisNeurotoxicityNrf2Perfluorooctanesulfonate (PFOS)ROS

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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.