Evidence map›Paper›PMID 19956437›Full record

ArticleAmerican journal of translational research2009

Triptolide induces anti-inflammatory cellular responses.

Ranyia Matta, Xianxi Wang, Hui Ge, William Ray, Leif D Nelin, Yusen Liu

Open access · greenAbstract read
In one paragraph

Article in American journal of translational research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
14.9field-weighted citation impact, top 2% 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

42 citing papers in PubMed, 75 citations in OpenAlex.

  1. Unraveling the Causal Linkages ofBioMed research international · 2026
    Article
  2. Liposome-Based Interventions in Knee Osteoarthritis.Small (Weinheim an der Bergstrasse, Germany) · 2025
    Review
  3. Review
  4. Article
  5. Triptolide induces PANoptosis in macrophages and causes organ injury in mice.Apoptosis : an international journal on programmed cell death · 2023
    Article
  6. Article
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  8. Article
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  10. Review
  11. Pharmacokinetics-Based Chronoefficacy ofFrontiers in pharmacology · 2021
    Article
  12. Review
  13. Review
  14. Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
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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

6 authors.

Ranyia Matta
Xianxi Wang
Hui Ge
William Ray
Leif D Nelin
Yusen Liu

Funding

The roles of MKP-1 in Gram-negative bacterial sepsis and colitisR01AI057798 · NIAID · RESEARCH INST NATIONWIDE CHILDREN'S HOSP · PI LIU, YUSEN · 2004 to 2010
$2.0M
Cationic Amino Acid Transporters and Lung NO ProductionR01HL075261 · NHLBI · RESEARCH INST NATIONWIDE CHILDREN'S HOSP · PI NELIN, LEIF D · 2006 to 2010
$1.6M
NHLBI NIH HHS R01 HL075261NIAID NIH HHS R01 AI057798
6 · The paper itself

Abstract

Tripterygium wilfordii Hook F. has been used for centuries in traditional Chinese medicine to treat rheumatoid arthritis, an autoimmune disease associated with increased production of the pro-inflammatory cytokine, tumor necrosis factor (TNF)-alpha. Triptolide is a compound originally purified from T. wilfordii Hook F. and has potent anti-inflammatory and immunosuppressant activities. In this study, we investigated the effect of triptolide on the global gene expression patterns of macrophages treated with lipopolysaccharide (LPS). We found that LPS stimulation resulted in >5-fold increase in expression of 117 genes, and triptolide caused a >50% inhibition in 47 of the LPS-inducible 117 genes. A large portion of the genes that were strongly induced by LPS and significantly inhibited by triptolide were pro-inflammatory cytokine and chemokine genes, including TNF-alpha, IL-1beta, and IL-6. Interestingly, LPS also induced the expression of micro-RNA-155 (miR-155) precursor, BIC, which was inhibited by triptolide. Confirming the cDNA array results, we demonstrated that triptolide blocked the induction of these pro-inflammatory cytokines as well as miR-155 in a dose-dependent manner. Profound inhibition of pro-inflammatory cytokine expression was observed at concentrations as low as 10-50 nM. However, triptolide neither inhibited the phosphorylation or degradation of IkappaBalpha after LPS stimulation, nor affected the DNA-binding activity of NF-kappaB. Surprisingly, we found that triptolide not only inhibited NF-kappaB-regulated reporter transcription, but also dramatically blocked the activity of other transcription factors. Our study offers a plausible explanation of the therapeutic mechanism of T. wilfordii Hook F.

Indexed as

Chinese medicinecytokinesInflammationrheumatoid arthritistranscriptionTripterygium wilfordii

Identifiers

PMID19956437
PMCPMC2776323
OpenAlexW108227102

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.