NSAID‐induced antral ulcers are associated with distinct changes in mucosal gene expression

Desai, Jaydev P.; Goo, Tyralee; Fukata, Masayuki; Sanyal, Shefali; Dikman, Andrew; Miller, Kenneth M.; Cohen, Lawrence B.; Brooks, Andrew I.; Wang, Qi; Abreu, María T.; Aisenberg, James

doi:10.1111/j.1365-2036.2009.04000.x

Cited by 6 publications

(5 citation statements)

References 60 publications

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“…This broad antioxidant effect may help to explain the fact that flavocoxid significantly down-regulated COX-2 gene expression in isolated human peripheral blood monocytes from OA patients whereas celecoxib, ibuprofen, and to a minor extent, acetaminophen, augmented COX-2 gene expression ( Figure 4 This was a surprising result since both traditional and selective COX-2 NSAIDs bind to and inhibit the COX enzyme production of inflammatory AA metabolites. Similar results have been found in patients who experience ulcerations in which COX-2 gene expression is up-regulated [90]. While this may be advantageous in maintaining prostaglandin E2 (PGE 2 ) production in the upper GI tract to mitigate ulcer formation, COX-2 gene induction could result in greater protein production generating elevated PG production associated with increased pain and inflammation.…”

Section: Ib Kinasesupporting

confidence: 66%

Flavocoxid (Limbrel ®) manages osteoarthritis through modification of multiple inflammatory pathways: a review

Burnett

Levy

2012

FFHD

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Limbrel (flavocoxid) is marketed as an FDA-regulated medical food for the clinical dietary management of osteoarthritis (OA) to be used under physician supervision. Flavocoxid is composed of a >90% mixture of baicalin and catechin and represents a non-targeted anti-inflammatory which works differently than non-steroidal anti-inflammatory drugs (NSAIDs) that bind to and only inhibit the cyclooxygenase moieties of COX-1 and COX-2. Flavocoxid binds to and weakly modulates the peroxidase activity of the COX enzymes permitting low level expression of prostaglandins (PGs), prostacyclin (PGI2) and thromboxane (TxA2). In addition, flavocoxid weakly inhibits phospholipase A2 (PLA2) and 5-lipoxygenase (5-LOX) as well as increases IϰBα and prevents nuclear factor kappa B (NFϰB) activation/induction of inflammatory genes such as tumor necrosis factor-alpha (TNFα), interleukin-1β (IL-1 β), IL-6, COX-2, inducible nitric oxide synthase (iNOS) and 5-LOX. In clinical studies, flavocoxid shows equivalent efficacy to naproxen with statistically fewer renal (edema) and upper gastrointestinal (GI) side effects, does not affect platelet function and bleeding times, does not change international normalized ratio (INR) in warfarinized patients, is well-tolerated in patients with previous NSAID-induced GI side effects, and decreases or eliminates the use of gastroprotective medications in patients who previously required them to tolerate NSAIDs. With its broad, non-targeted and multiple weak activities which result in fewer side effects compared to NSAIDs, flavocoxid represents a different way managing OA by working on the underlying and multiple causes of cartilage degradation as well as joint inflammation. Keywords: Flavocoxid, Limbrel, osteoarthritis, inflammatory pathways, and medical foods

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Section: Ib Kinasesupporting

confidence: 66%

Flavocoxid (Limbrel ®) manages osteoarthritis through modification of multiple inflammatory pathways: a review

Burnett

Levy

2012

FFHD

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“…This is contrary to the situation in humans, where NSAID-induced gastric ulceration occurs mainly in the gastric antrum [31]. For instance, naproxen is the most common and frequent NSAID used in rheumatoid arthritis patients, and the naproxen-induced gastropathy occurs mainly in the gastric antrum [31]. Using this experimental antral model of gastric ulcerations in rats to mimic the human scenario of complication risk after naproxen ingestion, Kim et al [32] have shown that the administration of naproxen caused the macro- and microscopic antral lesions and increased the tissue lipid peroxidation levels.…”

Section: Curcumin-induced Gastric Protection Against Nsaid-inducedmentioning

confidence: 78%

“…These lesions are recognized as bleeding erosions or lesions rather than typical ulcers [28]. This is contrary to the situation in humans, where NSAID-induced gastric ulceration occurs mainly in the gastric antrum [31]. For instance, naproxen is the most common and frequent NSAID used in rheumatoid arthritis patients, and the naproxen-induced gastropathy occurs mainly in the gastric antrum [31].…”

Section: Curcumin-induced Gastric Protection Against Nsaid-inducedmentioning

confidence: 99%

Curcumin: A Potent Protectant against Esophageal and Gastric Disorders

Kwiecień

Magierowski

Majka

et al. 2019

IJMS

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Turmeric obtained from the rhizomes of Curcuma longa has been used in the prevention and treatment of many diseases since the ancient times. Curcumin is the principal polyphenol isolated from turmeric, which exhibits anti-inflammatory, antioxidant, antiapoptotic, antitumor, and antimetastatic activities. The existing evidence indicates that curcumin can exert a wide range of beneficial pleiotropic properties in the gastrointestinal tract, such as protection against reflux esophagitis, Barrett’s esophagus, and gastric mucosal damage induced by nonsteroidal anti-inflammatory drugs (NSAIDs) and necrotizing agents. The role of curcumin as an adjuvant in the treatment of a Helicobacter pylori infection in experimental animals and humans has recently been proposed. The evidence that this turmeric derivative inhibits the invasion and proliferation of gastric cancer cells is encouraging and warrants further experimental and clinical studies with newer formulations to support the inclusion of curcumin in cancer therapy regimens. This review was designed to analyze the existing data from in vitro and in vivo animal and human studies in order to highlight the mechanisms of therapeutic efficacy of curcumin in the protection and ulcer healing of the upper gastrointestinal tract, with a major focus on addressing the protection of the esophagus and stomach by this emerging compound.

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“…It remains controversial whether gastric mucosal atrophy and duodenal metaplasia are reversible or not after eradication of the infection (62) . Furthermore, such possible mucosal alterations are difficult to confirm in consequence of not being possible, in the majority of cases, to obtain data on the previous conditions with respect to the presence of H. pylori in the population included in the studies (20,62) . Anatomopathological studies on peptic ulcers refer signs of inflammation in the regions surrounding the ulcer but not signs of mucosal atrophy (62) .…”

Section: Discussionmentioning

confidence: 99%

“…In order to be sure of the absence of the infectious cause of the peptic ulcer, it is also recommended that samples should be examined from both antrum and corpus, and utilizing two different tests, with negative results for both (62) . A lower bacterial density in the antrum can lead to false-negative urea respiratory tests (1,20,28,36) . It is general to endoscopic procedures that samples be taken from both antrum, where the majority of the ulcers reside, and corpus, where bacterial populations are higher.…”

Section: Discussionmentioning

confidence: 99%

ETIOPATHOGENESIS OF PEPTIC ULCER: back to the past?

Araujo

Borini

Guimarães

2014

Arq. Gastroenterol.

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-Objective -To review some aspects of the etiopathogenesis of peptic ulcerous disease especially on the basis of studies on its correlation with Helicobacter pylori (H. pylori). Methods -A search was made in the data bases MEDLINE, LILACS and PubMed, and in Brazilian and foreign books, referring to the incidence and prevalence of infection by H. pylori and of peptic ulcerous disease in various populations of different countries. Results -It was observed that the prevalence of H. pylori infection is similar in individuals with peptic ulcerous disease and the general population. There are differences between countries with respect to the prevalence of infection and of gastric or duodenal peptic ulcers. In many countries the prevalence of infection by H. pylori shows stability while the prevalence of peptic ulcerous disease is declining. The prevalence of peptic ulcerous disease without H. pylori infection varies between 20% and 56% in occidental countries. Discussion -The observations might be suggestive of H. pylori being only one more factor to be summed together with other aggressive components in the genesis of peptic ulcerous disease. We would therewith be returning to the classic concept that peptic gastric and duodenal ulcers have multifactorial etiology and would result from imbalance between aggressive and defensive factors. The focus of studies should be enriched with the identification of the defensive factors and of other aggressive factors besides the well known H. pylori and non-steroidal anti-inflammatory drugs, since these two aggressors do not exhaust the full causal spectrum. HEADINGS -Peptic ulcer. Stomach Ulcer. Duodenal ulcer. Helicobacter infections.

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NSAID‐induced antral ulcers are associated with distinct changes in mucosal gene expression

Abstract: SUMMARY BackgroundThe basis for individual variation in gastroduodenal vulnerability to NSAIDs is not well understood.

Cited by 6 publications

References 60 publications

Flavocoxid (Limbrel ®) manages osteoarthritis through modification of multiple inflammatory pathways: a review

Flavocoxid (Limbrel ®) manages osteoarthritis through modification of multiple inflammatory pathways: a review

Curcumin: A Potent Protectant against Esophageal and Gastric Disorders

ETIOPATHOGENESIS OF PEPTIC ULCER: back to the past?

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