Evidence map›Paper›PMID 27504095›Full record

ArticleFrontiers in pharmacology2016

A Standardized Chemically Modified Curcuma longa Extract Modulates IRAK-MAPK Signaling in Inflammation and Potentiates Cytotoxicity.

Minakshi Rana, Preeti Maurya, Sukka S Reddy, Vishal Singh, Hafsa Ahmad, Anil K Dwivedi, Madhu Dikshit, Manoj K Barthwal

Open access · goldAbstract read
In one paragraph

Article in Frontiers in pharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.2field-weighted citation impact, top 24% 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

11 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. Interplay of Interleukin-1Oncology research · 2026
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  3. Review
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  5. Standardized fraction of Xylocarpus moluccensis inhibits inflammation by modulating MAPK-NFκB and ROS-HIF1α-PKM2 activation.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022
    Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. 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

8 authors at 2 institutions in 1 country.

Minakshi RanaPharmacology Division, Council of Scientific and Industrial Research - Central Drug Research Institute Lucknow, India.
Preeti MauryaPharmacology Division, Council of Scientific and Industrial Research - Central Drug Research Institute Lucknow, India.
Sukka S ReddyPharmacology Division, Council of Scientific and Industrial Research - Central Drug Research Institute Lucknow, India.
Vishal SinghPharmacology Division, Council of Scientific and Industrial Research - Central Drug Research Institute Lucknow, India.
Hafsa AhmadDivision of Pharmaceutics, Council of Scientific and Industrial Research - Central Drug Research Institute Lucknow, India.
Anil K DwivediDivision of Pharmaceutics, Council of Scientific and Industrial Research - Central Drug Research Institute Lucknow, India.
Madhu DikshitPharmacology Division, Council of Scientific and Industrial Research - Central Drug Research Institute Lucknow, India.
Manoj K BarthwalPharmacology Division, Council of Scientific and Industrial Research - Central Drug Research Institute Lucknow, India.
Central Drug Research Institute · INCouncil of Scientific and Industrial Research · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The TLR/IL-1R pathway is a critical signaling module that is misregulated in pathologies like inflammation and cancer. Extracts from turmeric (Curcuma longa L.) enriched in curcumin and carbonyls like turmerones have been shown to exert potent anti-inflammatory effects. The present study evaluated the anti-inflammatory activity, cytotoxic effect and the underlying mechanism of a novel chemically modified, non-carbonyl compound enriched Curcuma longa L. (C. longa) extract (CMCE). CMCE (1 or 10 μg/mL; 14 h) significantly decreased LPS (50-100 ng/mL) induced TNF-α and IL-1β production in THP-1 cells, human, and mouse whole blood as measured by ELISA. LPS-induced IRAK1, MAPK activation, TLR4 expression, TLR4-MyD88 interaction, and IκBα degradation were significantly reduced in CMCE pre-treated THP-1 cells as assessed by Western blotting. CMCE (30, 100, and 300 mg/kg; 10 days p.o.) pre-treated and LPS (10 mg/kg) challenged Swiss mice exhibited attenuated plasma TNF-α, IL-1β, nitrite, aortic iNOS expression, and vascular dysfunction. In a PI permeability assay, cell lines derived from acute myeloid leukemia were most sensitive to the cytotoxic effects of CMCE. Analysis of Sub-G1 phase, Annexin V-PI positivity, loss of mitochondrial membrane potential, increased caspase-3, and PARP-1 activation confirmed CMCE induced apoptosis in HL-60 cells. IRAK inhibition also sensitized HL-60 cells to CMCE induced cytotoxicity. The present study defines the mechanism underlying the action of CMCE and suggests a therapeutic potential for its use in sepsis and leukemia.

Indexed as

caspase-3chemically modified Curcuma longa extractendotoxemiainterleukin-1 receptor-associated kinase 1mitochondrial membrane potential

Identifiers

PMID27504095
PMCPMC4959270
OpenAlexW2504141899

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.