Evidence map›Paper›PMID 29518056›Full record

ArticleNutrients2018

20(S)-Ginsenoside Rh2 Induce the Apoptosis and Autophagy in U937 and K562 Cells.

Jianjian Zhuang, Juxin Yin, Chaojian Xu, Ying Mu, Shaowu Lv

Open access · goldAbstract read
In one paragraph

Article in Nutrients, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
3.2field-weighted citation impact, top 7% 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

26 citing papers in PubMed, 63 citations in OpenAlex.

  1. Article
  2. Ginsenosides fromJournal of ginseng research · 2026
    Review
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  4. Anti-leukemia effects of ginsenoside monomer: A narrative review of pharmacodynamics study.Current therapeutic research, clinical and experimental · 2024
    Review
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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

5 authors at 2 institutions in 1 country.

Jianjian ZhuangKey Laboratory for Molecular Enzymology and Engineering of the Ministry of Education, College of Life Science, Jilin University, Changchun 130000, China. zhuangjianjian1234@163.com.
Juxin YinState Key Laboratory of Industrial Control Technology, Research Center for Analytical Instrumentation, Institute of Cyber-Systems and Control, Zhejiang University, Hangzhou 310000, China. yinjuxin@163.com.ORCID 0000-0002-4271-5157
Chaojian XuKey Laboratory for Molecular Enzymology and Engineering of the Ministry of Education, College of Life Science, Jilin University, Changchun 130000, China. cavalierxu@yeah.net.
Ying MuState Key Laboratory of Industrial Control Technology, Research Center for Analytical Instrumentation, Institute of Cyber-Systems and Control, Zhejiang University, Hangzhou 310000, China. muying@zju.edu.cn.
Shaowu LvKey Laboratory for Molecular Enzymology and Engineering of the Ministry of Education, College of Life Science, Jilin University, Changchun 130000, China. lvsw@jlu.edu.cn.
Jilin University · CNState Key Laboratory of Industrial Control Technology

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute myeloid leukemia (AML) and Chronic myelogenous leukemia (CML) are common leukemia in adults. 20(S)-GRh2 is an important bioactive substance that is present in Panax ginseng. However, there are no investigations that deal with the comparison of apoptosis, the occurrence of autophagy, and the relationship between apoptosis and autophagy after being treated with 20(S)-GRh2 in AML and CML. In this study, we explored the effect of 20(S)-GRh2 on the AML and CML (U937 and K562). Fluorescence microscopy, CCK-8, Quantitative realtime PCR, Western blot, transmission electron microscopy (TEM), and flow cytometric analysis were used to detect the occurrence of cell proliferation inhibition, apoptosis, and autophagy. By using the above methods, it was determined that apoptosis induced by 20(S)-GRh2 was more obvious in K562 than U937 cells and 20(S)-GRh2 could generate autophagy in K562 and U937 cells. When pretreated by a specific inhibitor of autophagy, (3-methyladenine), the 20(S)-GRh2-induced apoptosis was enhanced, which indicated that 20(S)-GRh2-induced autophagy may protect U937 and K562 cells from undergoing apoptotic cell death. On the other hand, pretreated by an apoptosis suppressor (Z-VAD-FMK), it greatly induced the autophagy and partially prevented 20(S)-GRh2 induced apoptosis. This phenomenon indicated that 20(S)-GRh2-induced autophagy may serve as a survival mechanism and apoptosis and autophagy could act as partners to induce cell death in a cooperative manner. These findings may provide a rationale for future clinical application by using 20(S)-GRh2 combined autophagy inhibitors for AML and CML.

Indexed as

ApoptosisAutophagyCell ProliferationGinsenosidesHumansK562 CellsReactive Oxygen SpeciesU937 Cellsginsenoside Rh2GinsenosidesReactive Oxygen Species20(S)-GRh2AMLapoptosisautophagyCMLcooperative manner

Identifiers

PMID29518056
PMCPMC5872746
OpenAlexW2793558613

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.