Evidence map›Paper›PMID 22067901›Full record

ArticleFree radical biology & medicine2012

Anti-inflammatory effects of benfotiamine are mediated through the regulation of the arachidonic acid pathway in macrophages.

Mohammad Shoeb, Kota V Ramana

Registry-linked trialOpen access · greenAbstract read
In one paragraph

Article in Free radical biology & medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03220113 (Safety and Efficacy of De-Novo Algorithm and Formula in the Treatment of Patients With Intractable Chronic Craniofacial Neuralgia, or Chronic Migraine Headaches.), which is not on this map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.4field-weighted citation impact, top 13% 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.

NCT03220113 phase1 / phase2unknown statusnot on this mapstarted 2017, after this paper: background citation

Safety and Efficacy of De-Novo Algorithm and Formula in the Treatment of Patients With Intractable Chronic Craniofacial Neuralgia, or Chronic Migraine Headaches.

TypeinterventionalSponsorCorona Doctors Medical Clinics, Inc.Ran2017 to 2019Enrolled100ConditionsChronic Migraine Without Aura, Intractable, Migraine With Typical Aura, Migraine DisordersArmsDexamethasone, Lidocaine, Thiamine cohort
3 · Its place in the literature

Who cites it

23 citing papers in PubMed, 71 citations in OpenAlex.

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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

2 authors at 1 institution in 1 country.

Mohammad ShoebDepartment of Biochemistry and Molecular Biology, University of Texas Medical Branch, Galveston, TX 77555, USA.
Kota V Ramana
The University of Texas Medical Branch at Galveston · US

Funding

Aldose Reductase: A Regulator of Inflammatory SignalsR01GM071036 · NIGMS · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI RAMANA, KOTA VENKATA · 2005 to 2011
$1.8M
NIGMS NIH HHS GM071036NIGMS NIH HHS R01 GM071036
6 · The paper itself

Abstract

Benfotiamine, a lipid-soluble analogue of vitamin B1, is a potent antioxidant that is used as a food supplement for the treatment of diabetic complications. Our recent study (U.C. Yadav et al., Free Radic. Biol. Med. 48:1423-1434, 2010) indicates a novel role for benfotiamine in the prevention of bacterial endotoxin, lipopolysaccharide (LPS)-induced cytotoxicity and inflammatory response in murine macrophages. Nevertheless, it remains unclear how benfotiamine mediates anti-inflammatory effects. In this study, we investigated the anti-inflammatory role of benfotiamine in regulating arachidonic acid (AA) pathway-generated inflammatory lipid mediators in RAW264.7 macrophages. Benfotiamine prevented the LPS-induced activation of cPLA2 and release of AA metabolites such as leukotrienes, prostaglandin E2, thromboxane 2 (TXB2), and prostacyclin (PGI2) in macrophages. Further, LPS-induced expression of AA-metabolizing enzymes such as COX-2, LOX-5, TXB synthase, and PGI2 synthase was significantly blocked by benfotiamine. Furthermore, benfotiamine prevented the LPS-induced phosphorylation of ERK1/2 and expression of transcription factors NF-κB and Egr-1. Benfotiamine also prevented the LPS-induced oxidative stress and protein-HNE adduct formation. Most importantly, compared to specific COX-2 and LOX-5 inhibitors, benfotiamine significantly prevented LPS-induced macrophage death and monocyte adhesion to endothelial cells. Thus, our studies indicate that the dual regulation of the COX and LOX pathways in AA metabolism could be a novel mechanism by which benfotiamine exhibits its potential anti-inflammatory response.

Indexed as

AnimalsAnti-Inflammatory AgentsArachidonic AcidCell AdhesionCell DeathCell LineCyclooxygenase 2DinoprostoneEpoprostenolExtracellular Matrix ProteinsExtracellular Signal-Regulated MAP KinasesGene ExpressionInflammationLeukotrienesLipopolysaccharidesMacrophagesAnti-Inflammatory AgentsArachidonic AcidbenphothiamineCyclooxygenase 2DinoprostoneEpoprostenolExtracellular Matrix ProteinsExtracellular Signal-Regulated MAP KinasesLeukotrienesLipopolysaccharidesLox protein, mouseNF-kappa BProtein-Lysine 6-OxidasePtgs2 protein, mouseThiamineThromboxane B2

Identifiers

PMID22067901
PMCPMC3249497
OpenAlexW2043422476

What OpenQuestion holds

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Registered trials

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.