Evidence map›Paper›PMID 23811723›Full record

ArticleActa pharmacologica Sinica2013

Emodin induces human T cell apoptosis in vitro by ROS-mediated endoplasmic reticulum stress and mitochondrial dysfunction.

Kai Qu, Nai-ying Shen, Xin-sen Xu, Hai-bo Su, Ji-chao Wei, Ming-hui Tai, Fan-di Meng, Lei Zhou, Yue-lang Zhang, Chang Liu

Open access · bronzeAbstract read
In one paragraph

Article in Acta pharmacologica Sinica, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

48 citing papers in PubMed, 93 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Polydatin: A natural compound with multifaceted anticancer properties.Journal of traditional and complementary medicine · 2025
    Review
  5. Immunometabolic Targets in CD8Liver cancer · 2025
    Review
  6. Article
  7. Review
  8. Article
  9. In Vitro Toxicity Assessment ofJournal of fungi (Basel, Switzerland) · 2024
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Emodin-Mediated Treatment of Acute Kidney Injury.Evidence-based complementary and alternative medicine : eCAM · 2022
    Review
  17. Mechanism of Emodin in the Treatment of Rheumatoid Arthritis.Evidence-based complementary and alternative medicine : eCAM · 2022
    Review
  18. Article
  19. Article
  20. Reactive Oxygen Species in Anticancer Immunity: A Double-Edged Sword.Frontiers in bioengineering and biotechnology · 2021
    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

10 authors at 3 institutions in 1 country.

Kai QuDepartment of Hepatobiliary Surgery, The First Affiliated Hospital of Medical College, Xi'an Jiaotong University, Xi'an 710061, China.
Nai-ying Shen
Xin-sen Xu
Hai-bo Su
Ji-chao Wei
Ming-hui Tai
Fan-di Meng
Lei Zhou
Yue-lang Zhang
Chang Liu
First Affiliated Hospital of Xi'an Jiaotong University · CNXi'an Jiaotong University · CNXian Yang Central Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimTo elucidate the molecular mechanisms underlying the immunosuppressive effects of emodin isolated from Rheum palmatum L.

methodsHuman T cells were isolated from the peripheral venous blood of 10 healthy adult donors. Cell viability was analyzed with MTT assay. AO/EB and Annexin V/PI staining and DNA damage assay were used to detect cell apoptosis. Fluorescence staining was used to detect the levels of ROS, the mitochondrial membrane potential and intracellular Ca(2+). Colorimetry was used to detect the levels of MDA and total SOD and GSH/GSSG ratio. The expression and activity of caspase-3, -4, and -9 were detected with Western blotting and a fluorometric assay. Western blotting was also used to detect the expression of Bcl-2, Bax, cytochrome C, and endoplasmic reticulum (ER) markers.

resultsEmodin (1, 10, and 100 μmol/L) inhibited the growth of human T cells and induced apoptosis in dose- and time dependent manners. Emodin triggered ER stress and significantly elevated intracellular free Ca(2+) in human T cells. It also disrupted mitochondrial membrane potential, and increased cytosolic level of cytochrome C, and the levels of activated cleavage fragments of caspase-3, -4, and -9 in human T cells. Furthermore, emodin significantly increased the levels of ROS and MDA, inhibited both SOD level and GSH/GSSG ratio in human T cells, whereas co-incubation with the ROS scavenger N-acetylcysteine (NAC, 20 μmol/L) almost completely blocked emodin-induced ER stress and mitochondrial dysfunction in human T cells, and decreased the caspase cascade-mediated apoptosis.

conclusionEmodin exerts immunosuppressive actions at least partly by inducing apoptosis of human T cells, which is triggered by ROS-mediated ER stress and mitochondrial dysfunction.

Indexed as

ApoptosisCell SurvivalDose-Response Relationship, DrugEmodinEndoplasmic Reticulum StressHumansLeukocytes, MononuclearMitochondriaReactive Oxygen SpeciesT-LymphocytesEmodinReactive Oxygen Species

Identifiers

PMID23811723
PMCPMC4003158
OpenAlexW2094300275

What OpenQuestion holds

Textmetadata
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.