Gastritis increases resistance to aspirin-induced mucosal injury via COX-2-mediated lipoxin synthesis

2003 ◽  
Vol 285 (1) ◽  
pp. G54-G61 ◽  
Author(s):  
Marcellus H. L. P. Souza ◽  
Octavio Menezes de Lima ◽  
Stella R. Zamuner ◽  
Stefano Fiorucci ◽  
John L. Wallace
Keyword(s):  
Drinking Water ◽  
Intravital Microscopy ◽  
Mucosal Injury ◽  
The Other ◽  
Gastric Damage ◽  
Protective Effects ◽  
Leukocyte Adherence ◽  
Mucosal Defense ◽  
Cox 2 ◽  
Normal Stomach

Products of cyclooxygenase (COX)-2 contribute to mucosal defense. Acetylation of COX-2 by aspirin has been shown to result in the generation of 15(R)-epi-lipoxin A4, which exerts protective effects in the stomach. In gastritis, it is possible that lipoxin A4 makes a greater contribution to mucosal defense. We tested this hypothesis in the rat, by using the iodoacetamide-induced gastritis model. Iodoacetamide was added to the drinking water for 5 days. Rats were then given aspirin, and the extent of gastric damage was blindly assessed 3 h later. Gastric 15(R)-epi-lipoxin A4 and PGE2 levels were determined. The effects of pretreatment with a selective COX-2 inhibitor, rofecoxib, and of a lipoxin receptor antagonist were assessed. Effects of aspirin and the other test drugs on leukocyte adherence within mesenteric venules were assessed by intravital microscopy. Aspirin elicited greater lipoxin synthesis in the inflamed than in the normal stomach, and there was reduced gastric damage. Rofecoxib inhibited lipoxin synthesis and exacerbated aspirin-induced damage. The lipoxin antagonist also exacerbated aspirin-induced damage. In rats with gastritis, aspirin reduced leukocyte adherence (in contrast to an increase in normal rats), and this effect was reversed by rofecoxib or by the lipoxin antagonist. These results support the notion that aspirin-triggered lipoxin synthesis via COX-2 makes an important contribution to mucosal defense in both the normal and inflamed stomach.

Aspirin, but not NO-releasing aspirin (NCX-4016), interacts with selective COX-2 inhibitors to aggravate gastric damage and inflammation

2004 ◽  
Vol 286 (1) ◽  
pp. G76-G81 ◽  
Author(s):  
John L. Wallace ◽  
Stella R. Zamuner ◽  
Webb McKnight ◽  
Michael Dicay ◽  
Andrea Mencarelli ◽  
...  
Keyword(s):  
Repeated Administration ◽  
Mucosal Injury ◽  
Gastric Damage ◽  
Attractive Alternative ◽  
Myeloperoxidase Activity ◽  
Protective Effects ◽  
Cox 2 ◽  
Nitric Oxide Releasing ◽  
Cox 2 Inhibitors ◽  
Ncx 4016

Aceylation of cyclooxygenase (COX)-2 by aspirin can trigger the formation of 15(R)-epilipoxin A4, or aspirin-triggered lipoxin (ATL). ATL exerts protective effects in the stomach. Selective COX-2 inhibitors block ATL synthesis and exacerbate aspirin-induced gastric damage. Nitric oxide-releasing aspirins, including NCX-4016, have antiplatelet effects similar to aspirin but do not cause gastric damage. In the present study, we examined whether or not NCX-4016 triggers ATL synthesis and/or upregulates gastric COX-2 expression and the effects of coadministration of NCX-4016 with a selective COX-2 inhibitor on gastric mucosal injury and inflammation. Rats were given aspirin or NCX-4016 orally and either vehicle or a selective COX-2 inhibitor (celecoxib) intraperitoneally. Gastric damage was blindly scored, and granulocyte infiltration into gastric tissue was monitored through measurement of myeloperoxidase activity. Gastric PG and ATL synthesis was measured as was COX-2 expression. Whereas celecoxib inhibited gastric ATL synthesis and increased the severity of aspirin-induced gastric damage and inflammation, coadministration of celecoxib and NCX-4016 did not result in damage or inflammation. NCX-4016 did not upregulate gastric COX-2 expression nor did it trigger ATL synthesis (in contrast to aspirin). Daily administration of aspirin for 5 days resulted in significantly less gastric damage than that seen with a single dose, as well as augmented ATL synthesis. Celecoxib reversed this effect. In contrast, repeated administration of NCX-4016 failed to cause gastric damage, whether given alone or with celecoxib. These studies support the notion that NCX-4016 may be an attractive alternative to aspirin for indications such as cardioprotection, including in individuals also taking selective COX-2 inhibitors.

Temporal variability of disinfection by-products concentration in urban public water system

2013 ◽  
Vol 14 (4) ◽  
pp. 393-398
Keyword(s):  
Drinking Water ◽  
Water Samples ◽  
Temporal Variability ◽  
Water System ◽  
The Other ◽  
Major Constituent ◽  
System P ◽  
Public Water System ◽  
Drinking Water Samples ◽  
By Products

The occurrence of trihalomethanes (THMs) was studied in the drinking water samples from urban water supply network of Karachi city that served more than 18 million people. Drinking water samples were collected from 58 locations in summer (May-August) and winter (November-February) seasons. The major constituent of THMs detected was chloroform in winter (92.34%) and summer (93.07%), while the other THMs determined at lower concentrations. Summer and winter concentrations of total THMs at places exceed the levels regulated by UEPA (80 μg l-1) and WHO (100 μg l-1). GIS linked temporal variability in two seasons showed significantly higher median concentration (2.5%-23.06%) of THMs compared to winter.

Enteric viruses in drinking water supplies

2002 ◽  
Vol 2 (3) ◽  
pp. 17-22
Author(s):  
A.P. Wyn-Jones ◽  
J. Watkins ◽  
C. Francis ◽  
M. Laverick ◽  
J. Sellwood
Keyword(s):  
Drinking Water ◽  
Heavy Rainfall ◽  
Liquid Culture ◽  
Plaque Assay ◽  
Enteric Viruses ◽  
Enteric Virus ◽  
The Other ◽  
Raw Water ◽  
Rt Pcr ◽  
Water Supplies

Two rural spring drinking water supplies were studied for their enteric virus levels. In one, serving about 30 dwellings, the water was chlorinated before distribution; in the other, which served a dairy and six dwellings the water was not treated. Samples of treated (40 l) and untreated (20 l) water were taken under normal and heavy rainfall conditions over a six weeks period and concentrated by adsorption/elution and organic flocculation. Infectious enterovirus in concentrates was detected in liquid culture and enumerated by plaque assay, both in BGM cells, and concentrates were also analysed by RT-PCR. Viruses were found in both raw water supplies. Rural supplies need to be analysed for viruses as well as bacterial and protozoan pathogens if the full microbial hazard is to be determined.

scholarly journals Protective effects of glycoglycerolipids extracted from spinach on 5-fluorouracil induced intestinal mucosal injury

2010 ◽  
Vol 57 (3,4) ◽  
pp. 314-320 ◽  
Author(s):  
Asuka Shiota ◽  
Takahiko Hada ◽  
Tomoko Baba ◽  
Minako Sato ◽  
Hisami Yamanaka-Okumura ◽  
...  
Keyword(s):  
Mucosal Injury ◽  
Protective Effects ◽  
Intestinal Mucosal Injury

scholarly journals Evaluation of the best vaccination regimen against Gumboro disease, based on the histopathologic lesions of bursa of Fabricius, in broilers

2018 ◽  
Vol 52 (2) ◽  
pp. 135
Author(s):  
B. BOUYIOUKLIS (Π. ΜΠΟΥΓΙΟΥΚΛΗΣ) ◽  
S. LEKKAS (Σ. ΛΕΚΚΑΣ) ◽  
I. GEORGOPOULOU (Ι. ΓΕΩΡΓΟΠΟΥΛΟΥ) ◽  
P. IORDANIDIS (Π. ΙΟΡΔΑΝΙΔΗΣ)
Keyword(s):  
Drinking Water ◽  
Disease Virus ◽  
Vaccine Strain ◽  
The Other ◽  
Field Strain ◽  
Bursa Of Fabricius ◽  
Control Group ◽  
Vaccination Regimen ◽  
Experimental Animals ◽  
Gumboro Disease

For the evaluation of the best vaccination regimen against Gumboro disease using the vaccine strain D-78, based on the histopathologic lesions of bursa of Fabricius, 5 groups of experimental animals (A, B, C, D, E) of 15 chicks each were used. The chicks of group Β received the D-78 vaccine strain with the drinking water at the age of 14 days, those of C at the age of 8 and 11 days, and those of D at the age of 8 and 16 days, while the chicks of the other groups (A and E) remained unvaccinated. In the following, the chicks of the A, B, C and D groups were infected with a field strain of Gumboro disease virus, while those of E remained unvaccinated and uninfected as a control group. After 10 days, all chicks were killed and their bursae examined histological. It was established that the histopathologic lesions to the bursae of group C chicks were of a slighter degree than those of all the other challenged groups and therefore the protection to bursa of Fabricius against the disease is better with this vaccination regimen.

Protective effects of somatostatin against gastric damage induced by hemorrhagic shock, stress and PAF in the rat

1993 ◽  
Vol 47 (2) ◽  
pp. 195-203 ◽  
Author(s):  
John L. Wallace ◽  
Elisabeth Boichot ◽  
Carole Sidoti ◽  
Alain Brecx ◽  
Monique Paubert-Braquet
Keyword(s):  
Hemorrhagic Shock ◽  
Gastric Damage ◽  
Protective Effects ◽  
Shock Stress

scholarly journals Eplerenone inhibits aldosterone-induced renal expression of cyclooxygenase

2012 ◽  
Vol 13 (3) ◽  
pp. 353-359 ◽  
Author(s):  
MA Bayorh ◽  
A Rollins-Hairston ◽  
J Adiyiah ◽  
D Lyn ◽  
D Eatman
Keyword(s):  
Salt Intake ◽  
High Salt ◽  
Prostaglandin E ◽  
Renal Tubules ◽  
Protective Effects ◽  
High Salt Diet ◽  
Salt Diet ◽  
High Salt Intake ◽  
Low Salt ◽  
Cox 2

Introduction: The upregulation of cyclooxygenase (COX) expression by aldosterone (ALDO) or high salt diet intake is very interesting and complex in the light of what is known about the role of COX in renal function. Thus, in this study, we hypothesize that apocynin (APC) and/or eplerenone (EPL) inhibit ALDO/salt-induced kidney damage by preventing the production of prostaglandin E2 (PGE2). Methods: Dahl salt-sensitive rats on either a low-salt or high-salt diet were treated with ALDO (0.2 mg pellet) in the presence of EPL (100 mg/kg/day) or APC (1.5 mM). Indirect blood pressure, prostaglandins and ALDO levels and histological changes were measured. Results: Cyclooxygenase-2 (COX-2) levels were upregulated in the renal tubules and peritubular vessels after high-salt intake, and APC attenuated renal tubular COX-2 protein expression induced by ALDO. Plasma PGE2 levels were significantly reduced by ALDO in the rats fed a low-salt diet when compared to rats fed a high-salt diet. PGE2 was blocked by EPL but increased in the presence of APC. Conclusions: The beneficial effects of EPL may be associated with an inhibition of PGE2. The mechanism underlying the protective effects of EPL is clearly distinct from that of APC and suggests that these agents can have differential roles in cardiovascular disease.

scholarly journals Role of Cox-2 in Vascular Inflammation: An Experimental Model of Metabolic Syndrome

2013 ◽  
Vol 2013 ◽  
pp. 1-10 ◽  
Author(s):  
Nicolás F. Renna ◽  
Emiliano R. Diez ◽  
Carina Lembo ◽  
Roberto M. Miatello
Keyword(s):  
Oxidative Stress ◽  
Metabolic Syndrome ◽  
Drinking Water ◽  
Experimental Model ◽  
Vascular Remodeling ◽  
Vascular Inflammation ◽  
Left Ventricular ◽  
Wky Rats ◽  
Cox 2

The objective of this work was to demonstrate the role of COX-2 enzyme at the vascular in experimental model of metabolic syndrome. SHR male WKY rats were employed; they were distributed in 8 groups (n=8each): control (W); W + L: WKY rats receiving 20 mg/kg of lumiracoxib by intraesophageal administration; SHR; SHR + L: SHR + 20 mg/kg of lumiracoxib by intraesophageal administration; Fructose-Fed Rats (FFR): WKY rats receiving 10% (w/v) fructose solution in drinking water during all 12 weeks; FFR + L: FFR + 20 mg/kg of lumiracoxib by intraesophageal administration; Fructose-Fed Hypertensive Rats (FFHR): SHR receiving 10% (w/v) fructose solution in drinking water during all 12 weeks; and FFHR + L: FFHR + 20 mg/kg of lumiracoxib by intraesophageal administration. Metabolic variables, blood pressure, morphometric variables, and oxidative stress variables were evaluated; also MMP-2 and MMP-9 (collagenases), VCAM-1, and NF-κB by Westernblot or IFI were evaluated. FFHR presented all variables of metabolic syndrome; there was also an increase in oxidative stress variables; vascular remodeling and left ventricular hypertrophy were evidenced along with a significant increase in the expression of the mentioned proinflammatory molecules and increased activity and expression of collagenase. Lumiracoxib was able to reverse vascular remodeling changes and inflammation, demonstrating the involvement of COX-2 in the pathophysiology of vascular remodeling in this experimental model.

Case of flexor tenosynovitis caused by Mycobacterium arupense

2021 ◽  
Vol 14 (10) ◽  
pp. e245130
Author(s):  
Kushali Patel ◽  
John Flaherty
Keyword(s):  
Drinking Water ◽  
Case Report ◽  
Water Systems ◽  
The Other ◽  
Empiric Antibiotic Therapy ◽  
Joint Infections ◽  
Empiric Antibiotic ◽  
Environmental Pathogens ◽  
Fish Tanks ◽  
Flexor Tenosynovitis

Mycobacterium arupense is a member of the Mycobacterium terrae complex (MTC) that is implicated in bone and joint infections, among others. This group of environmental pathogens can be found in soil, reclaimed and drinking water systems, rodents, fish tanks and bioaerosols in duck houses. Interestingly, while M. arupense is genotypically closely related to the other agents in the MTC, antibiotic susceptibility of these mycobacteria can vary widely and empiric antibiotic therapy is controversial. Our case report contributes to the very limited literature on M. arupense tenosynovitis—as only six cases have been reported since 2008—and sheds light on different courses of treatment. While previous cases have been successfully treated, a streamlined course of therapy for M. arupense tenosynovitis is still needed.

Sign in / Sign up

Export Citation Format

Share Document