Evidence map›Paper›PMID 30454068›Full record

ArticleJournal of experimental & clinical cancer research : CR2018

Compound kushen injection suppresses human acute myeloid leukaemia by regulating the Prdxs/ROS/Trx1 signalling pathway.

Yanxia Jin, Qian Yang, Li Liang, Lu Ding, Yuxing Liang, Dongdong Zhang, Balu Wu, Tian Yang, Hailing Liu, Tingting Huang and 6 more

Open access · goldAbstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.8field-weighted citation impact, top 8% 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

31 citing papers in PubMed, 60 citations in OpenAlex.

  1. Article
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  5. Role of reactive oxygen species in myelodysplastic syndromes.Cellular & molecular biology letters · 2024
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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

16 authors at 3 institutions in 1 country.

Yanxia JinDepartment of Haematology, Zhongnan Hospital, Wuhan University, No. 169 Donghu Road, Wuchang District, Wuhan, 430071, Hubei Province, China.
Qian YangDepartment of Haematology, Zhongnan Hospital, Wuhan University, No. 169 Donghu Road, Wuchang District, Wuhan, 430071, Hubei Province, China.
Li LiangKey Laboratory of Artificial Micro- and Nano-Structures of Ministry of Education, School of Physics and Technology, Wuhan University, Wuhan, 430072, Hubei, China.
Lu DingDepartment of Haematology, Zhongnan Hospital, Wuhan University, No. 169 Donghu Road, Wuchang District, Wuhan, 430071, Hubei Province, China.
Yuxing LiangDepartment of Haematology, Zhongnan Hospital, Wuhan University, No. 169 Donghu Road, Wuchang District, Wuhan, 430071, Hubei Province, China.
Dongdong ZhangDepartment of Haematology, Zhongnan Hospital, Wuhan University, No. 169 Donghu Road, Wuchang District, Wuhan, 430071, Hubei Province, China.
Balu WuDepartment of Haematology, Zhongnan Hospital, Wuhan University, No. 169 Donghu Road, Wuchang District, Wuhan, 430071, Hubei Province, China.
Tian YangDepartment of Radiation and Medical Oncology, Zhongnan Hospital of Wuhan University, Wuhan, 430071, Hubei, China.
Hailing LiuDepartment of Clinical Haematology, Second Affiliated Hospital, Medical School of Xi'an Jiaotong University, Xi'an, 710004, Shaanxi, China.
Tingting HuangDepartment of Haematology, Zhongnan Hospital, Wuhan University, No. 169 Donghu Road, Wuchang District, Wuhan, 430071, Hubei Province, China.
Hui ShenDepartment of Haematology, Zhongnan Hospital, Wuhan University, No. 169 Donghu Road, Wuchang District, Wuhan, 430071, Hubei Province, China.
Honglei TuDepartment of Haematology, Zhongnan Hospital, Wuhan University, No. 169 Donghu Road, Wuchang District, Wuhan, 430071, Hubei Province, China.
Yunbao PanDepartment of Laboratory Medicine, Zhongnan Hospital, Wuhan University, Wuhan, 430071, Hubei, China.
Yongchang WeiDepartment of Radiation and Medical Oncology, Zhongnan Hospital of Wuhan University, Wuhan, 430071, Hubei, China.
Yi YangKey Laboratory of Artificial Micro- and Nano-Structures of Ministry of Education, School of Physics and Technology, Wuhan University, Wuhan, 430072, Hubei, China.
Fuling ZhouDepartment of Haematology, Zhongnan Hospital, Wuhan University, No. 169 Donghu Road, Wuchang District, Wuhan, 430071, Hubei Province, China. zhoufuling@whu.edu.cn.
Zhongnan Hospital of Wuhan University · CNWuhan University · CNSecond Affiliated Hospital of Xi'an Jiaotong University · CN

Funding

the Natural Science Foundation of China (NSFC) programme 81770179Zhongnan Hospital of Wuhan University Science, Technology and Innovation Seed Fund cxpy20160001Zhongnan Hospital of Wuhan University Science, Technology and Innovation Seed Fund cxpy20160012
6 · The paper itself

Abstract

backgroundThe increase in the levels of reactive oxygen species (ROS) in acute myeloid leukemia (AML) patients has been previously described; thus, it is important to regulate ROS levels in AML.

methodsFlow cytometry were used to assess the in vitro effect of compound kushen injection (CKI). Quantitative proteomics were used to analyse the mechanism. The AML patient-derived xenograft (PDX) model were used to evaluate the in vivo effect of CKI.

resultsWe found that intracellular ROS levels in AML cells were decreased, the antioxidant capacity were increased when treated with CKI. CKI inhibited the proliferation of AML cells and enhanced the cytotoxicity of AML cells, which has few toxic effects on haematopoietic stem cells (HSCs) and T cells. At the single-cell level, individual AML cells died gradually by CKI treatment on optofluidic chips. CKI promoted apoptosis and arrested cell cycle at G1/G0 phase in U937 cells. Furthermore, higher peroxiredoxin-3 (Prdx3) expression levels were identified in CKI-treated U937 cells through quantitative proteomics detection. Mechanically, the expression of Prdx3 and peroxiredoxin-2 (Prdx2) was up-regulated in CKI-treated AML cells, while thioredoxin 1 (Trx1) was reduced. Laser confocal microscopy showed that the proteins Prdx2 could be Interacted with Trx1 by CKI treatment. In vivo, the survival was longer and the disease was partially alleviated by decreased CD45+ immunophenotyping in peripheral blood in the CKI-treated group in the AML PDX model.

conclusionsAntioxidant CKI possess better clinical application against AML through the Prdxs/ROS/Trx1 signalling pathway.

Indexed as

AnimalsApoptosisCell ProliferationDisease Models, AnimalDrugs, Chinese HerbalFemaleHeterograftsHL-60 CellsHumansLeukemia, Myeloid, AcuteMiceMicroscopy, ConfocalPeroxiredoxinsReactive Oxygen SpeciesSignal TransductionThioredoxinsDrugs, Chinese HerbalkushenPeroxiredoxinsPRDX2 protein, humanReactive Oxygen SpeciesThioredoxinsTXN protein, humanAcute myeloid leukaemiaCompound kushen injectionPeroxiredoxin-2Peroxiredoxin-3Reactive oxygen species

Identifiers

PMID30454068
PMCPMC6245615
OpenAlexW2901786434

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Registered trials

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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.