Evidence map›Paper›PMID 22245632›Full record

ArticlePhytochemistry2012

The inhibition of lipopolysaccharide-induced macrophage inflammation by 4 compounds in Hypericum perforatum extract is partially dependent on the activation of SOCS3.

Nan Huang, Ludmila Rizshsky, Catherine C Hauck, Basil J Nikolau, Patricia A Murphy, Diane F Birt

Abstract read
In one paragraph

Article in Phytochemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

20 citing papers in PubMed, 34 citations in OpenAlex.

  1. Chemopreventive mechanisms of amentoflavone: recent trends and advancements.Naunyn-Schmiedeberg's archives of pharmacology · 2023
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  12. Antiatopic Dermatitis Effect of Artemisia iwayomogi in Dust Mice Extract-Sensitized Nc/Nga Mice.Evidence-based complementary and alternative medicine : eCAM · 2014
    Article
  13. Article
  14. Article
  15. A survey of chinese medicinal herbal treatment for chemotherapy-induced oral mucositis.Evidence-based complementary and alternative medicine : eCAM · 2013
    Review
  16. Article
  17. 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 at 1 institution in 1 country.

Nan HuangThe Center for Research on Botanical Dietary Supplements, Iowa State University, Ames, IA 50011, United States. huangnan@iastate.edu
Ludmila Rizshsky
Catherine C Hauck
Basil J Nikolau
Patricia A Murphy
Diane F Birt
Iowa State University · US

Funding

SEPARATIONS/STRUCTURE/BIOAVAILABILITY/KRAUS, GEORGEP50AT004155 · NCCIH · IOWA STATE UNIVERSITY · PI BIRT, DIANE FEICKERT · 2007 to 2010
$4.5M
NCCIH NIH HHS 9P50AT004155NCCIH NIH HHS P50 AT004155
6 · The paper itself

Abstract

Our previous studies found that 4 compounds, namely pseudohypericin, amentoflavone, quercetin, and chlorogenic acid, in Hypericum perforatum ethanol extract synergistically inhibited lipopolysaccharide (LPS)-induced macrophage production of prostaglandin E2 (PGE2). Microarray studies led us to hypothesize that these compounds inhibited PGE2 production by activating suppressor of cytokine signaling 3 (SOCS3). In the current study, siRNA was used to knockdown expression of SOCS3 in RAW 264.7 macrophages and investigated the impact of H. perforatum extract and the 4 compounds on inflammatory mediators and cytokines. It was found that the SOCS3 knockdown significantly compromised the inhibition of PGE2 and nitric oxide (NO) by the 4 compounds, but not by the extract. The 4 compounds, but not the extract, decreased interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α), while both lowered interleukine-1β. SOCS3 knockdown further decreased IL-6 and TNF-α. Pseudohypericin was the major contributor to the PGE2 and NO inhibition in cells treated with the 4 compounds, and its activity was lost with the SOCS3 knockdown. Cyclooxygenase-2 (COX-2) and inducible NO synthase protein expression were not altered by the treatments, while COX-2 activity was decreased by the extract and the 4 compounds and increased by SOCS3 knockdown. In summary, it was demonstrated that the 4 compounds inhibited LPS-induced PGE2 and NO through SOCS3 activation. The reduction of PGE2 can be partially attributed to COX-2 enzyme activity, which was significantly elevated with SOCS3 knockdown. At the same time, these results also suggest that constituents in H. perforatum extract were alleviating LPS-induced macrophage response through SOCS3 independent mechanisms.

Indexed as

AnimalsAnti-Inflammatory AgentsBiflavonoidsCell LineChlorogenic AcidCytokinesDinoprostoneEthanolGene Knockdown TechniquesHypericumInflammationInflammation MediatorsLipopolysaccharidesMacrophagesMiceNitric OxideamentoflavoneAnti-Inflammatory AgentsBiflavonoidsChlorogenic AcidCytokinesDinoprostoneEthanolInflammation MediatorsLipopolysaccharidesNitric OxidePerylenepseudohypericinQuercetinRNA, Small InterferingSocs3 protein, mouseSuppressor of Cytokine Signaling 3 ProteinSuppressor of Cytokine Signaling Proteins

Identifiers

PMID22245632
PMCPMC3294117
OpenAlexW2078342606

What OpenQuestion holds

Textmetadata
LicenceTDM
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.