Evidence map›Paper›PMID 14691050›Full record

ArticleBritish journal of pharmacology2004

Coupling of boswellic acid-induced Ca2+ mobilisation and MAPK activation to lipid metabolism and peroxide formation in human leucocytes.

Anja Altmann, Daniel Poeckel, Lutz Fischer, Manfred Schubert-Zsilavecz, Dieter Steinhilber, Oliver Werz

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in British journal of pharmacology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.1field-weighted citation impact, top 14% 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

14 citing papers in PubMed, 50 citations in OpenAlex.

  1. International journal of molecular sciences · 2026
    Article
  2. Review
  3. The journey of boswellic acids from synthesis to pharmacological activities.Naunyn-Schmiedeberg's archives of pharmacology · 2024
    Review
  4. Review
  5. Effect ofIranian journal of basic medical sciences · 2020
    Review
  6. Antioxidant, anti-inflammatory and anti-fibrotic effects ofExperimental and therapeutic medicine · 2020
    Article
  7. Article
  8. Drug-Herb Interactions in the Elderly Patient with IBD: a Growing Concern.Current treatment options in gastroenterology · 2017
    Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
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 at 1 institution in 1 country.

Anja AltmannInstitute of Pharmaceutical Chemistry, University of Frankfurt, Marie-Curie Strasse 9, Frankfurt D-60439, Germany.
Daniel Poeckel
Lutz Fischer
Manfred Schubert-Zsilavecz
Dieter Steinhilber
Oliver Werz
Goethe University Frankfurt · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

1. We have previously shown that 11-keto boswellic acids (11-keto-BAs), the active principles of Boswellia serrata gum resins, activate p38 MAPK and p42/44(MAPK) and stimulate Ca(2+) mobilisation in human polymorphonuclear leucocytes (PMNL). 2. In this study, we attempted to connect the activation of MAPK and mobilisation of Ca(2+) to functional responses of PMNL, including the formation of reactive oxygen species (ROS), release of arachidonic acid (AA), and leukotriene (LT) biosynthesis. 3. We found that, in PMNL, 11-keto-BAs stimulate the formation of ROS and cause release of AA as well as its transformation to LTs via 5-lipoxygenase. 4. Based on inhibitor studies, 11-keto-BA-induced ROS formation is Ca(2+)-dependent and is mediated by NADPH oxidase involving PI 3-K and p42/44(MAPK) signalling pathways. Also, the release of AA depends on Ca(2+) and p42/44(MAPK), whereas the pathways stimulating 5-LO are not readily apparent. 5. Pertussis toxin, which inactivates G(i/0) protein subunits, prevents MAPK activation and Ca(2+) mobilisation induced by 11-keto-BAs, implying the involvement of a G(i/0) protein in BA signalling. 6. Expanding studies on differentiated haematopoietic cell lines (HL60, Mono Mac 6, BL41-E-95-A) demonstrate that the ability of BAs to activate MAPK and to mobilise Ca(2+) may depend on the cell type or the differentiation status. 7. In summary, we conclude that BAs act via G(i/0) protein(s) stimulating signalling pathways that control functional leucocyte responses, in a similar way as chemoattractants, that is, N-formyl-methionyl-leucyl-phenylalanine or platelet-activating factor.

Indexed as

Calcium SignalingDose-Response Relationship, DrugEnzyme ActivationHL-60 CellsHumansLeukocytesLipid PeroxidesMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinasesp38 Mitogen-Activated Protein KinasesReactive Oxygen SpeciesTriterpenesboswellic acidLipid PeroxidesMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinasesp38 Mitogen-Activated Protein KinasesReactive Oxygen SpeciesTriterpenes

Identifiers

PMID14691050
PMCPMC1574191
OpenAlexW2020990519

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.