Evidence map›Paper›PMID 36139782›Full record

ArticleAntioxidants (Basel, Switzerland)2022

Hesperidin Protects SH-SY5Y Neuronal Cells against High Glucose-Induced Apoptosis via Regulation of MAPK Signaling.

Chaemoon Lim, Ao Xuan Zhen, Sungwoo Ok, Pincha Devage Sameera Madushan Fernando, Herath Mudiyanselage Udari Lakmini Herath, Mei Jing Piao, Kyoung Ah Kang, Jin Won Hyun

Open access · goldAbstract read
In one paragraph

Article in Antioxidants (Basel, Switzerland), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
4.2field-weighted citation impact, top 5% 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

17 citing papers in PubMed, 30 citations in OpenAlex.

  1. Untargeted Metabolomic and Phytochemical Profiling ofPharmaceuticals (Basel, Switzerland) · 2026
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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 2 institutions in 1 country.

Chaemoon LimDepartment of Orthopedic Surgery, Jeju National University Hospital, College of Medicine, Jeju National University, Jeju 63241, Korea.ORCID 0000-0002-1252-9425
Ao Xuan ZhenDepartment of Biochemistry, College of Medicine, Jeju National University, Jeju 63243, Korea.
Sungwoo OkDepartment of Orthopedic Surgery, Jeju National University Hospital, College of Medicine, Jeju National University, Jeju 63241, Korea.ORCID 0000-0002-3623-2167
Pincha Devage Sameera Madushan FernandoDepartment of Biochemistry, College of Medicine, Jeju National University, Jeju 63243, Korea.
Herath Mudiyanselage Udari Lakmini HerathDepartment of Biochemistry, College of Medicine, Jeju National University, Jeju 63243, Korea.
Mei Jing PiaoJeju Research Center for Natural Medicine, Jeju National University, Jeju 63243, Korea.
Kyoung Ah KangJeju Research Center for Natural Medicine, Jeju National University, Jeju 63243, Korea.
Jin Won HyunDepartment of Biochemistry, College of Medicine, Jeju National University, Jeju 63243, Korea.ORCID 0000-0002-3403-3762
Jeju National University · KRJeju National University Hospital · KR

Funding

Jeju National University Hospital 2021
6 · The paper itself

Abstract

Neurodegenerative diseases are associated with neuronal cell death through apoptosis. Apoptosis is tightly associated with the overproduction of reactive oxygen species (ROS), and high glucose levels contribute to higher oxidative stress in diabetic patients. Hesperidin, a natural active compound, has been reported to scavenge free radicals. Only a few studies have explored the protective effects of hesperidin against high glucose-induced apoptosis in SH-SY5Y neuronal cells. Glucose stimulated neuronal cells to generate excessive ROS and caused DNA damage. In addition, glucose triggered endoplasmic reticulum stress and upregulated cytoplasmic as well as mitochondrial calcium levels. Hesperidin inhibited glucose-induced ROS production and mitigated the associated DNA damage and endoplasmic reticulum stress. The downregulation of antiapoptotic protein Bcl-2 following glucose treatment was reversed by a hesperidin treatment. Furthermore, hesperidin repressed the glucose-induced Bcl-2-associated X protein, cleaved caspase-9, and cleaved caspase-3. Hesperidin also suppressed the glucose-induced phosphorylation of extracellular signal-regulated kinase and c-Jun N-terminal kinase. The current results confirmed that hesperidin could protect neuronal cells against glucose-induced ROS. Mechanistically, hesperidin was shown to promote cell viability via attenuation of the mitogen-activated protein kinase signaling pathway.

Indexed as

apoptosisglucosehesperidinoxidative stressSH−SY5Y neuronal cell

Identifiers

PMID36139782
PMCPMC9495902
OpenAlexW4293686629

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.