Evidence map›Paper›PMID 31906464›Full record

ArticleMolecules (Basel, Switzerland)2020

Ginsenoside Re Mitigates 6-Hydroxydopamine-Induced Oxidative Stress through Upregulation of GPX4.

Gyeong Hee Lee, Won Jin Lee, Jinwoo Hur, Eunsu Kim, Hyuk Gyoon Lee, Han Geuk Seo

Open access · goldAbstract read
In one paragraph

Article in Molecules (Basel, Switzerland), 2020. 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
1.9field-weighted citation impact, top 14% 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, 38 citations in OpenAlex.

  1. Article
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  10. Article
  11. Review
  12. Pharmacological Properties of Ginsenoside Re.Frontiers in pharmacology · 2022
    Review
  13. Article
  14. Review
  15. Iron Metabolism and Ferroptosis in Epilepsy.Frontiers in neuroscience · 2020
    Review
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

6 authors at 1 institution in 1 country.

Gyeong Hee LeeDepartment of Food Science and Biotechnology of Animal Resources, College of Sang-Huh Life Science, Konkuk University, 120 Neungdong-ro, Gwangjin-Gu, Seoul 05029, Korea.
Won Jin LeeDepartment of Food Science and Biotechnology of Animal Resources, College of Sang-Huh Life Science, Konkuk University, 120 Neungdong-ro, Gwangjin-Gu, Seoul 05029, Korea.
Jinwoo HurDepartment of Food Science and Biotechnology of Animal Resources, College of Sang-Huh Life Science, Konkuk University, 120 Neungdong-ro, Gwangjin-Gu, Seoul 05029, Korea.
Eunsu KimDepartment of Food Science and Biotechnology of Animal Resources, College of Sang-Huh Life Science, Konkuk University, 120 Neungdong-ro, Gwangjin-Gu, Seoul 05029, Korea.
Hyuk Gyoon LeeDepartment of Food Science and Biotechnology of Animal Resources, College of Sang-Huh Life Science, Konkuk University, 120 Neungdong-ro, Gwangjin-Gu, Seoul 05029, Korea.
Han Geuk SeoDepartment of Food Science and Biotechnology of Animal Resources, College of Sang-Huh Life Science, Konkuk University, 120 Neungdong-ro, Gwangjin-Gu, Seoul 05029, Korea.
Konkuk University · KR

Funding

Korea Institute of Planning and Evaluation for Technology in Food, Agriculture and Forestry 318028-03-2
6 · The paper itself

Abstract

Ginsenosides are active components found abundantly in ginseng which has been used as a medicinal herb to modify disease status for thousands of years. However, the pharmacological activity of ginsenoside Re in the neuronal system remains to be elucidated. Neuroprotective activity of ginsenoside Re was investigated in SH-SY5Y cells exposed to 6-hydroxydopamine (6-OHDA) to induce cellular injury. Ginsenoside Re significantly inhibited 6-OHDA-triggered cellular damage as judged by analysis of tetrazolium dye reduction and lactose dehydrogenase release. In addition, ginsenoside Re induced the expression of the antioxidant protein glutathione peroxidase 4 (GPX4) but not catalase, glutathione peroxidase 1, glutathione reductase, or superoxide dismutase-1. Furthermore, upregulation of GPX4 by ginsenoside Re was mediated by phosphoinositide 3-kinase and extracellular signal-regulated kinase but not by p38 mitogen-activated protein kinase or c-Jun N-terminal kinase. Ginsenoside Re also suppressed 6-OHDA-triggered cellular accumulation of reactive oxygen species and peroxidation of membrane lipids. The GPX4 inhibitor (1S,3R)-RSL3 reversed ginsenoside Re-mediated inhibition of cellular damage in SH-SY5Y cells exposed to 6-OHDA, indicating that the neuronal activity of ginsenoside Re is due to upregulation of GPX4. These findings suggest that ginsenoside Re-dependent upregulation of GPX4 reduces oxidative stress and thereby alleviates 6-OHDA-induced neuronal damage.

Indexed as

CatalaseCell Line, TumorCell SurvivalGinsenosidesGlutathione PeroxidaseGlutathione Peroxidase GPX1Glutathione ReductaseHumansLipid PeroxidationMolecular StructureOxidative StressOxidopaminePhospholipid Hydroperoxide Glutathione PeroxidaseReactive Oxygen SpeciesSuperoxide Dismutase-1Catalaseginsenoside ReGinsenosidesGlutathione PeroxidaseGlutathione Peroxidase GPX1Glutathione ReductaseGPX1 protein, humanOxidopaminePhospholipid Hydroperoxide Glutathione PeroxidaseReactive Oxygen SpeciesSuperoxide Dismutase-1ginsenoside Reglutathione peroxidase 4neuronal damageoxidative stressSH-SY5Y cells

Identifiers

PMID31906464
PMCPMC6983050
OpenAlexW2998433454

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.