Evidence map›Paper›PMID 32557145›Full record

ArticleJournal of molecular neuroscience : MN2021

Naringin Targets NFKB1 to Alleviate Oxygen-Glucose Deprivation/Reoxygenation-Induced Injury in PC12 Cells Via Modulating HIF-1α/AKT/mTOR-Signaling Pathway.

Wei Cao, She-Jun Feng, Min-Chen Kan

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of molecular neuroscience : MN, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.1field-weighted citation impact, top 20% 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

15 citing papers in PubMed, 26 citations in OpenAlex.

  1. Review
  2. Article
  3. Naringin Suppresses CoClAntioxidants (Basel, Switzerland) · 2025
    Article
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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

3 authors at 2 institutions in 1 country.

Wei CaoNeurology Ward 3, Affiliated Hospital of Hebei University, Baoding, 071000, Hebei, China.
She-Jun FengDepartment of Neurology, Handan Central Hospital, No.15 Zhonghua South Street, Handan, 056001, Hebei, China.
Min-Chen KanDepartment of Neurology, Handan Central Hospital, No.15 Zhonghua South Street, Handan, 056001, Hebei, China. tuo56g@163.com.ORCID http://orcid.org/0000-0001-7379-0814
Handan College · CNAffiliated Hospital of Hebei University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

This study was designed to investigate the effect of naringin in oxygen-glucose deprivation/reoxygenation (OGD/R) model and its mechanism. The target gene of naringin and the enriched pathways of the gene were searched and identified using bioinformatics analysis. Then OGD/R model was built using PC12 cells, after which the cells were treated with different concentrations of naringin. Subsequently, cell proliferation and apoptosis were evaluated by cell counting kit-8 (CCK-8) and flow cytometry assays, respectively. Meanwhile, the expression of NFKB1 in PC12 cells underwent OGD/R-induced injury was detected by qRT-PCR, while apoptosis-related and pathway-related proteins were checked by Western blot. DCF-DA kit was utilized to measure the level of ROS. Our results revealed that NFKB1, which was upregulated in MACO rats and OGD/R-treated PC12 cells, was a target gene of naringin. Naringin could alleviate OGD/R-induced injury via promoting the proliferation, and repressing the apoptosis of PC12 cells through regulating the expression of NFKB1 and apoptosis-associated proteins and ROS level. Besides, the depletion of NFKB1 was positive to cell proliferation but negative to cell apoptosis. Moreover, the depletion of NFKB1 enhanced the influences of naringin on cell proliferation and apoptosis as well as the expression of apoptosis-related proteins and ROS level. Western blotting indicated that both naringin treatment and depletion of NFKB1 could increase the expression of HIF-1α, p-AKT, and p-mTOR compared with OGD/R group. What's more, treatment by naringin and si-NFKB1 together could significantly increase these effects. Nevertheless, the expression of AKT and mTOR among each group was almost not changed. In conclusion, naringin could prevent the OGD/R-induced injury in PC12 cells in vitro by targeting NFKB1 and regulating HIF-1α/AKT/mTOR-signaling pathway, which might provide novel ideas for the therapy of cerebral ischemia-reperfusion (I/R) injury.

Indexed as

AnimalsApoptosisbcl-2-Associated X ProteinCell DivisionFlavanonesGene Expression RegulationGene OntologyGlucoseHypoxia-Inducible Factor 1, alpha SubunitInfarction, Middle Cerebral ArteryNF-kappa B p50 SubunitOxygenPC12 CellsPhytotherapyProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-bcl-2Bax protein, ratbcl-2-Associated X ProteinFlavanonesGlucoseHif1a protein, ratHypoxia-Inducible Factor 1, alpha SubunitmTOR protein, ratnaringinNF-kappa B p50 SubunitOxygenProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-bcl-2Reactive Oxygen SpeciesRNA, Small InterferingTOR Serine-Threonine KinasesApoptosisHIF-1α/AKT/mTOR-signaling pathwayNaringinNFKB1OGD/R-induced injuryProliferation

Identifiers

PMID32557145
OpenAlexW3035775206

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.