Evidence map›Paper›PMID 37298981›Full record

ArticleMolecules (Basel, Switzerland)2023

Naringenin Induces HepG2 Cell Apoptosis via ROS-Mediated JAK-2/STAT-3 Signaling Pathways.

Ming Zhang, Jianmei Lai, Qianlong Wu, Jia Lai, Jingyao Su, Bing Zhu, Yinghua Li

Open access · goldAbstract read
In one paragraph

Article in Molecules (Basel, Switzerland), 2023. 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
6.2field-weighted citation impact, top 3% 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, 27 citations in OpenAlex.

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  15. The Essential Oil fromPharmaceuticals (Basel, Switzerland) · 2023
    Article
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

7 authors at 1 institution in 1 country.

Ming ZhangDepartment of Interventional Radiology and Vascular Anomalies, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou 510120, China.
Jianmei LaiCenter Laboratory, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou 510120, China.ORCID 0009-0008-9270-3403
Qianlong WuCenter Laboratory, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou 510120, China.ORCID 0000-0003-2407-9326
Jia LaiCenter Laboratory, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou 510120, China.
Jingyao SuCenter Laboratory, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou 510120, China.
Bing ZhuCenter Laboratory, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou 510120, China.
Yinghua LiCenter Laboratory, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou 510120, China.ORCID 0000-0002-6271-8283
Guangzhou Medical University · CN

Funding

Guangdong Natural Science Foundation 2020A1515110648Open Fund of Guangdong Provincial Key Laboratory of Functional Supramolecular Coordination Materials and Applications 2020A03Open Project of Guangdong Key Laboratory of Marine Materia Medica LMM2020-7Science and Technology Planning Project of Guangzhou 202201020655 and 202102010202
6 · The paper itself

Abstract

Hepatocarcinoma is one of the most prevalent digestive system tumors worldwide and lacks effective therapy. Recently, naringenin has been isolated from some citrus fruits, and its anticancer effects have been tested. However, the molecular mechanisms of naringenin and the potential implications of oxidative stress in naringenin-induced cytotoxicity in HepG2 cells remain elusive. Based on the above, the present study examined the effect of naringenin on the cytotoxic and anticancer mechanisms of HepG2 cells. Naringenin-induced HepG2 cell apoptosis was confirmed via the accumulation of the sub-G1 cell population, phosphatidylserine exposure, mitochondrial transmembrane potential loss, DNA fragmentation, caspase-3 activation, and caspase-9 activation. Furthermore, naringenin enhanced cytotoxic effects on HepG2 cells and triggered intracellular reactive oxygen species; the signaling pathways of JAK-2/STAT-3 were inhibited, and caspase-3 was activated to advance cell apoptosis. These results suggest that naringenin plays an important role in inducing apoptosis in HepG2 cells and that naringenin may be a promising candidate for cancer therapy.

Indexed as

Antineoplastic AgentsLiver NeoplasmsApoptosisCaspase 3FlavanonesHep G2 CellsHumansMembrane Potential, MitochondrialReactive Oxygen SpeciesSignal TransductionAntineoplastic AgentsCaspase 3FlavanonesnaringeninReactive Oxygen Speciesapoptosiscancercaspase-3naringeninROS

Identifiers

PMID37298981
PMCPMC10254813
OpenAlexW4379232328

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.