Evidence map›Paper›PMID 33215356›Full record

ArticleCellular and molecular neurobiology2021

Involvement of α7nAChR in the Protective Effects of Genistein Against β-Amyloid-Induced Oxidative Stress in Neurons via a PI3K/Akt/Nrf2 Pathway-Related Mechanism.

Jianbin Guo, Guoqing Yang, Yuqing He, Huiming Xu, Hong Fan, Jing An, Lingling Zhang, Rui Zhang, Guihua Cao, Dingjun Hao and 1 more

Open access · greenAbstract read
In one paragraph

Article in Cellular and molecular neurobiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
4.5field-weighted citation impact, top 4% 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

25 citing papers in PubMed, 57 citations in OpenAlex.

  1. Article
  2. Nrf2 signaling pathway and its molecular regulatory mechanism.Journal of Zhejiang University. Science. B · 2026
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  16. Biological aspects in controlling angiogenesis: current progress.Cellular and molecular life sciences : CMLS · 2022
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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 5 institutions in 1 country.

Jianbin Guo *Department of Joint Surgery, Hong Hui Hospital, Xi'an Jiaotong University, Xi'an, 710054, China.ORCID http://orcid.org/0000-0002-9956-4097
Guoqing Yang *Department of Anesthesiology, The Second Affiliated Hospital of Shaanxi University of Traditional Chinese Medicine, Xianyang, 712000, Shaanxi, China.ORCID http://orcid.org/0000-0002-9825-4660
Yuqing He *School of Basic Medicine, Ningxia Medical University, Yinchuan, 750004, China.ORCID http://orcid.org/0000-0002-8141-3549
Huiming XuStem Cell Research Center, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, 200127, China.ORCID http://orcid.org/0000-0003-4823-6920
Hong FanDepartment of Spine Surgery, Hong Hui Hospital, Xi'an Jiaotong University, Xi'an, 710054, China.ORCID http://orcid.org/0000-0003-4987-2582
Jing AnTranslational Medicine Center, Hong Hui Hospital, Xi'an Jiaotong University, Xi'an, 710054, China.ORCID http://orcid.org/0000-0002-6535-6054
Lingling ZhangTranslational Medicine Center, Hong Hui Hospital, Xi'an Jiaotong University, Xi'an, 710054, China.ORCID http://orcid.org/0000-0001-7555-8138
Rui ZhangTranslational Medicine Center, Hong Hui Hospital, Xi'an Jiaotong University, Xi'an, 710054, China.ORCID http://orcid.org/0000-0002-8664-6915
Guihua CaoDepartment of Geriatrics, Xijing Hospital, The Fourth Military Medical University, Xi'an, 710069, China.ORCID http://orcid.org/0000-0001-9205-2315
Dingjun HaoDepartment of Spine Surgery, Hong Hui Hospital, Xi'an Jiaotong University, Xi'an, 710054, China. haodingjun@126.com.ORCID http://orcid.org/0000-0001-9006-0901
Hao YangTranslational Medicine Center, Hong Hui Hospital, Xi'an Jiaotong University, Xi'an, 710054, China. yanghao.71_99@yahoo.com.ORCID http://orcid.org/0000-0002-1144-0584
Xi'an Honghui Hospital · CNAffiliated Hospital of Shaanxi University of Chinese Medicine · CNNingxia Medical University · CNRenji Hospital · CNXijing Hospital · CN

Funding

National Natural Science Foundation of China 81571208National Natural Science Foundation of China 81772357National Natural Science Foundation of China 81830077National Natural Science Foundation of China 82071551Natural Science Foundation of Shaanxi Province 2020JM-686Xi'an Science and Technology Research Project 2019114913YX004SF037(3)
6 · The paper itself

Abstract

Abnormal excessive production and deposition of β-amyloid (Aβ) peptides in selectively susceptible brain regions are thought to be a key pathogenic mechanism underlying Alzheimer's disease (AD), resulting in memory deficits and cognitive impairment. Genistein is a phytoestrogen with great promise for counteracting diverse Aβ-induced insults, including oxidative stress and mitochondrial dysfunction. However, the exact molecular mechanism or mechanisms underlying the neuroprotective effects of genistein against Aβ-induced insults are largely uncharacterized. To further elucidate the possible mechanism(s) underlying these protective effects, we investigated the neuroprotective effects of genistein against Aβ-induced oxidative stress mediated by orchestrating α7 nicotinic acetylcholine receptor (α7nAChR) signaling in rat primary hippocampal neurons. Genistein significantly increased cell viability, reduced the number of apoptotic cells, decreased accumulation of reactive oxygen species (ROS), decreased contents of malondialdehyde (MDA) and lactate dehydrogenase (LDH), upregulated BCL-2 expression, and suppressed Caspase-3 activity occurring after treatment with 25 μM Aβ25-35. Simultaneously, genistein markedly inhibited the decreases in α7nAChR mRNA and protein expression in cells treated with Aβ25-35. In addition, α7nAChR signaling was intimately involved in the genistein-mediated activation of phosphatidylinositol 3-kinase (PI3K)/Akt and Nrf2/keap1 signaling. Thus, α7nAChR activity together with the PI3K/Akt/Nrf2 signaling cascade likely orchestrates the molecular mechanism underlying the neuroprotective effects of genistein against Aβ-induced oxidative injury.

Indexed as

alpha7 Nicotinic Acetylcholine ReceptorAmyloid beta-PeptidesAnimalsGenisteinHippocampusKelch-Like ECH-Associated Protein 1Models, BiologicalNecroptosisNeuronsNeuroprotective AgentsNF-E2-Related Factor 2Oxidative StressPeptide FragmentsPhosphatidylinositol 3-KinasePhosphorylationProto-Oncogene Proteins c-aktalpha7 Nicotinic Acetylcholine ReceptorAmyloid beta-Peptidesamyloid beta-protein (25-35)GenisteinKelch-Like ECH-Associated Protein 1Neuroprotective AgentsNF-E2-Related Factor 2Peptide FragmentsPhosphatidylinositol 3-KinaseProto-Oncogene Proteins c-aktGenisteinHippocampal neuronOxidative stressPI3K/Akt/Nrf2α7 Nicotinic acetylcholine receptorβ-Amyloid peptide

Identifiers

PMID33215356
PMCPMC11448600
OpenAlexW3104913539

What OpenQuestion holds

Textmetadata
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Registered trials

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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.