scholarly journals Preventive but Not Curative Efficacy of Celecoxib on Bladder Carcinogenesis in a Rat Model

2010 ◽  
Vol 2010 ◽  
pp. 1-11 ◽  
Author(s):  
José Sereno ◽  
Belmiro Parada ◽  
Flávio Reis ◽  
Fernanda X. Cunha ◽  
Edite Teixeira-Lemos ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Rat Model ◽  
Preventive Treatment ◽  
Inhibitory Effect ◽  
Cyclooxygenase 2 ◽  
Curative Treatment ◽  
Male Wistar Rats ◽  
Cox 2 ◽  
Cancer Inhibition

To evaluate the effect of a cyclooxygenase 2 inhibitor, celecoxib (CEL), on bladder cancer inhibition in a rat model, when used as preventive versus as curative treatment. The study comprised 52 male Wistar rats, divided in 5 groups, during a 20-week protocol: control: vehicle, carcinogen: 0.05% ofN-butyl-N-(4-hydroxybutyl) nitrosamine (BBN), CEL: 10 mg/kg/day of the selective COX-2 inhibitor Celebrex, preventive CEL (CEL+BBN-P), and curative CEL (BBN+CEL-C) groups. Although tumor growth was markedly inhibited by the preventive application of CEL, it was even aggravated by the curative treatment. The incidence of gross bladder carcinoma was: control 0/8(0%), BBN 13/20(65%), CEL 0/8(0%), CEL+BBN-P 1/8(12.5%), and BBN+CEL-C 6/8(75%). The number and volume of carcinomas were significantly lower in the CEL+BBN-P versus BBN, accompanied by an ample reduction in hyperplasia, dysplasia, and papillary tumors as well as COX-2 immunostaining. In spite of the reduction of tumor volumes in the curative BBN+CEL-C group, tumor malignancy was augmented. An anti-inflammatory and antioxidant profile was encountered only in the group under preventive treatment. In conclusion, preventive, but not curative, celecoxib treatment promoted a striking inhibitory effect on bladder cancer development, reinforcing the potential role of chemopreventive strategies based on cyclooxygenase 2 inhibition.

scholarly journals Streptococcus suis Induces Expression of Cyclooxygenase-2 in Porcine Lung Tissue

2021 ◽  
Vol 9 (2) ◽  
pp. 366
Author(s):  
Muriel Dresen ◽  
Josephine Schenk ◽  
Yenehiwot Berhanu Weldearegay ◽  
Désirée Vötsch ◽  
Wolfgang Baumgärtner ◽  
...  
Keyword(s):  
Lung Tissue ◽  
Streptococcus Suis ◽  
Cyclooxygenase 2 ◽  
Economic Losses ◽  
Biological Processes ◽  
Alveolar Tissue ◽  
Cox 2 ◽  
Ciliated Epithelial Cells ◽  
Immunohistological Analysis

Streptococcus suis is a common pathogen colonising the respiratory tract of pigs. It can cause meningitis, sepsis and pneumonia leading to economic losses in the pig industry worldwide. Cyclooxygenase-2 (COX-2) and its metabolites play an important regulatory role in different biological processes like inflammation modulation and immune activation. In this report we analysed the induction of COX-2 and the production of its metabolite prostaglandin E2 (PGE2) in a porcine precision-cut lung slice (PCLS) model. Using Western blot analysis, we found a time-dependent induction of COX-2 in the infected tissue resulting in increased PGE2 levels. Immunohistological analysis revealed a strong COX-2 expression in the proximity of the bronchioles between the ciliated epithelial cells and the adjacent alveolar tissue. The morphology, location and vimentin staining suggested that these cells are subepithelial bronchial fibroblasts. Furthermore, we showed that COX-2 expression as well as PGE2 production was detected following infection with two prevalent S. suis serotypes and that the pore-forming toxin suilysin played an important role in this process. Therefore, this study provides new insights in the response of porcine lung cells to S. suis infections and serves as a basis for further studies to define the role of COX-2 and its metabolites in the inflammatory response in porcine lung tissue during infections with S. suis.

scholarly journals The role of cyclooxygenase-2 on endurance exercise training in female LDL-receptor knockout ovariectomized mice

2013 ◽  
Vol 85 (3) ◽  
pp. 1157-1164 ◽  
Author(s):  
FLAVIA DE OLIVEIRA ◽  
LAURA B.M. MAIFRINO ◽  
GUSTAVO P.P. DE JESUS ◽  
JULIANA G. CARVALHO ◽  
CLAUDIA MARCHON ◽  
...  
Keyword(s):  
Cardiovascular Risk ◽  
Exercise Training ◽  
Ldl Receptor ◽  
Density Lipoprotein ◽  
Cyclooxygenase 2 ◽  
Sedentary Control ◽  
Down Regulation ◽  
Ovariectomized Mice ◽  
Cox 2

Estrogen deprivation in postmenopausal women increases cardiovascular risk. Cardiovascular risk as a result of atherosclerosis is able to induce an inflammatory disease as far as cyclooxygenase-2 ( COX-2) expression. The purpose of the study was to investigate the role of COX-2 on exercise training in female mice low-density lipoprotein receptor knockout ( LDL-KO) with or without ovariectomy. A total of 15 female C57BL/6 mice and 15 female LDL-KO mice were distributed into 6 groups: sedentary control, sedentary control ovariectomized, trained control ovariectomized, LDL-KO sedentary, LDL-KO sedentary ovariectomized and LDL-KO trained ovariectomized. The ascending part of the aorta was stained with H&E and COX-2 expression was assessed by immunohistochemistry. Results revealed that ovariectomy as well as exercise training were not able to induce histopathological changes in mouse aorta for all groups investigated. LDL-KO mice demonstrated plaque containing cholesterol clefts, foamy histiocytes and mild inflammatory process for all groups indistinctly. Ovariectomy induced a strong immunoexpression in atherosclerosis lesion of LDL-KO mice. Nevertheless, a down-regulation of COX-2 expression was detected in LDL-KO trained ovariectomized when compared to LDL-KO sedentary. Our results are consistent with the notion that exercise training is able to modulate COX-2 expression in LDL-KO mice as a result of COX-2 down-regulation.

scholarly journals The Role of Propolis in Pulp Pain by Inhibiting Cyclooxygenase-2 Expression

2021 ◽  
Vol 11 (1) ◽  
pp. 11
Author(s):  
Ira Widjiastuti ◽  
Widya Saraswati ◽  
Annisa Rahma
Keyword(s):  
Side Effects ◽  
Pain Relief ◽  
Inflammatory Pain ◽  
Cyclooxygenase 2 ◽  
Propolis Extract ◽  
In Silico Studies ◽  
Cox 2

Background: Inflammation of the pulp can lead to elicit pain. Pain in inflammation is induced by the cyclooxygenase-2 enzyme (COX-2) which induces prostaglandin E2 (PGE2) resulting in pain. Pain in the pulp can be relieved by eugenol. In its application, eugenol is toxic to pulp fibroblasts. Due to the side effect, it is worth considering other biocompatible materials with minimal side effects, such as propolis. Flavonoids and phenolic acids that contained in propolis can inhibit COX-2. Therefore, an analysis outlined in the literature review is needed to examine the results of research related to the role of propolis as pulp pain relief by inhibiting COX-2 expression. Purpose: To analyze the role of propolis in pulp pain by inhibiting COX-2 expression. Reviews: Propolis extract that extracted by ethanol, water, and hydroalcohol has pain relief properties in the pulp by inhibiting COX-2 by directly binding to the COX-2 receptors and by reducing the production of proinflammatory cytokines which are COX-2 inducers, proven through in vivo, in vitro, and in silico studies in various target cell organs. Conclusion: Propolis extract has high prospect as inflammatory pain inhibitor in the pulp by inhibit COX-2 expression.

Role of cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2) derived prostaglandins (PG) in adaptive cytoprotection induced by mild stress

1998 ◽  
Vol 114 ◽  
pp. A82
Author(s):  
T. Brzozowski ◽  
P.C. Konturek ◽  
R. Pajdo ◽  
N. Nagraba ◽  
A. Szczeklik ◽  
...  
Keyword(s):  
Cyclooxygenase 2 ◽  
Mild Stress ◽  
Adaptive Cytoprotection ◽  
Cyclooxygenase 1 ◽  
Cox 2 ◽  
Cox 1

A role for cyclooxygenase-2 in lipopolysaccharide-induced anorexia in rats

2002 ◽  
Vol 283 (4) ◽  
pp. R862-R868 ◽  
Author(s):  
F. Lugarini ◽  
B. J. Hrupka ◽  
G. J. Schwartz ◽  
C. R. Plata-Salaman ◽  
W. Langhans
Keyword(s):  
Cerebrospinal Fluid ◽  
Cyclooxygenase 2 ◽  
Major Metabolite ◽  
Time Dependent ◽  
Selective Inhibitors ◽  
Cox 2 ◽  
Cox 1

Because nonselective cycloooxygenase (COX) inhibition attenuated anorexia after lipopolysaccharide (LPS) administration, we tested the ability of resveratrol (2.5, 10, and 40 mg/kg) and NS-398 (2.5, 10, and 40 mg/kg), selective inhibitors of the two COX isoforms COX-1 and -2, respectively, to attenuate LPS (100 μg/kg ip)-induced anorexia. NS-398 (10 and 40 mg/kg) administered with LPS at lights out attenuated LPS-induced anorexia, whereas resveratrol at all doses tested did not. Because prostaglandin (PG) E2 is considered the major metabolite synthesized by COX, we measured plasma and cerebrospinal fluid (CSF) PGE2levels after LPS administration. LPS induced a time-dependent increase of PGE2 in CSF but not in plasma. NS-398 (5, 10, and 40 mg/kg) blocked the LPS-induced increase in CSF PGE2, whereas resveratrol (10 mg/kg) did not. These results support a role of COX-2 in mediating the anorectic response to peripheral LPS and point at PGE2 as a potential neuromodulator involved in this response.

scholarly journals Omega-3 Fatty Acids Inhibit Tumor Growth in a Rat Model of Bladder Cancer

2013 ◽  
Vol 2013 ◽  
pp. 1-11 ◽  
Author(s):  
Belmiro Parada ◽  
Flávio Reis ◽  
Raquel Cerejo ◽  
Patrícia Garrido ◽  
José Sereno ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Bladder Cancer ◽  
Rat Model ◽  
Redox Status ◽  
Omega 3 Fatty Acids ◽  
Omega 3 ◽  
Markers Of Inflammation ◽  
Male Wistar Rats ◽  
Serum Crp

Omega-3 (ω-3) fatty acids have been tested on prevention and treatment of several cancer types, but the efficacy on “in vivo” bladder cancer has not been analyzed yet. This study aimed at evaluating the chemopreventive efficacy of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) mixture in an animal model of bladder cancer. Forty-four male Wistar rats were divided into 4 groups during a 20-week protocol: control; carcinogen—N-butyl-N-(4-hydroxybutyl) nitrosamine (BBN);ω-3 (DHA + EPA); andω-3 + BBN. BBN andω-3 were given during the initial 8 weeks. At week 20 blood and bladder were collected and checked for the presence of urothelium lesions and tumors, markers of inflammation, proliferation, and redox status. Incidence of bladder carcinoma was, control (0%),ω-3 (0%), BBN (65%), andω-3 + BBN (62.5%). Theω-3 + BBN group had no infiltrative tumors or carcinomain situ, and tumor volume was significantly reduced compared to the BBN (0.9 ± 0.1 mm3versus 112.5 ± 6.4 mm3). Also, it showed a reduced MDA/TAS ratio and BBN-induced serum CRP, TGF-β1, and CD31 were prevented. In conclusion, omega-3 fatty acids inhibit the development of premalignant and malignant lesions in a rat model of bladder cancer, which might be due to anti-inflammatory, antioxidant, anti-proliferative, and anti-angiogenic properties.

1004 INHIBITION OF CYCLOOXYGENASE-2 (COX-2); AN OPPORTUNITY FOR BLADDER CANCER CONTROL

2009 ◽  
Vol 8 (4) ◽  
pp. 371
Author(s):  
S. Kontos ◽  
A. Kominea ◽  
G. Koritsiadis ◽  
V. Simaioforidis ◽  
S. Koritsiadis ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Cancer Control ◽  
Cyclooxygenase 2 ◽  
Cox 2

Cyclooxygenase-2 expression in Warthin's tumour

2005 ◽  
Vol 119 (7) ◽  
pp. 515-518 ◽  
Author(s):  
A H C Loy ◽  
T C Putti ◽  
L K S Tan
Keyword(s):  
Quantitative Analysis ◽  
Parotid Gland ◽  
Immunohistochemical Staining ◽  
Cyclooxygenase 2 ◽  
Duct System ◽  
Salivary Duct ◽  
Epithelial Component ◽  
Warthin’S Tumour ◽  
Cox 2

Objectives: To determine whether cyclooxygenase-2 (COX-2) is overexpressed in Warthin's tumours, and to characterize its pattern of expression.Methods: Twenty-one paraffin-embedded Warthin's tumour specimens were analysed by immunohistochemical staining for expression of human COX-2. Semi-quantitative analysis of the staining was performed.Results: In all of the specimens, we found that there was overexpression of COX-2 within the epithelial component of the tumours, with no expression in the lymphoid components. There was also overexpression of COX-2 in the salivary duct system of normal parotid tissue.Conclusions: Our results suggest that COX-2 is up-regulated in the epithelial component of Warthin's tumours. Our findings support the hypothesis that Warthin's tumours originate from heterotopic ductal epithelial cells of the parotid gland. The role of COX-2 expression in the pathogenesis of Warthin's tumours remains to be determined.

scholarly journals ApoL1 renal risk variants induce aberrant THP-1 monocyte differentiation and increase eicosanoid production via enhanced expression of cyclooxygenase-2

2018 ◽  
Vol 315 (1) ◽  
pp. F140-F150 ◽  
Author(s):  
Hewang Lee ◽  
Hila Roshanravan ◽  
Ying Wang ◽  
Koji Okamoto ◽  
Junghwa Ryu ◽  
...  
Keyword(s):  
Gene Expression ◽  
Specific Inhibitor ◽  
Cyclooxygenase 2 ◽  
Prostaglandin E ◽  
Monocyte Differentiation ◽  
Eicosanoid Production ◽  
Gene And Protein Expression ◽  
Cox 2 ◽  
Tgf Β1

Apolipoprotein L1 ( ApoL1) genetic variants are strongly associated with kidney diseases. We investigated the role of ApoL1 variants in monocyte differentiation and eicosanoid production in macrophages, as activated tissue macrophages in kidney might contribute to kidney injury. In human monocyte THP-1 cells, transient overexpression of ApoL1 (G0, G1, G2) by transfection resulted in a 5- to 11-fold increase in CD14 and CD68 gene expression, similar to that seen with phorbol-12-myristate acetate treatment. All ApoL1 variants caused monocytes to differentiate into atypical M1 macrophages with marked increase in M1 markers CD80, TNF, IL1B, and IL6 and modest increase in the M2 marker CD163 compared with control cells. ApoL1-G1 transfection induced additional CD206 and TGFB1 expression, and ApoL1-G2 transfection induced additional CD204 and TGFB1 expression. Gene expression of prostaglandin E2 (PGE2) synthase and thromboxane synthase and both gene and protein expression of cyclooxygenase-2 (COX-2) were increased by ApoL1-G1 and -G2 variants compared with -G0 transfection. Higher levels of PGE2 and thromboxane B2, a stable metabolite of thromboxane A2, and transforming growth factor (TGF)-β1 were released into the supernatant of cultured THP-1 cells transfected with ApoL1-G1 and -G2, but not -G0. The increase in PGE2, thromboxane B2, and TGF-β1 was inhibited by COX-2-specific inhibitor CAY10404 but not by COX-1-specific inhibitor SC-560. These results demonstrate a novel role of ApoL1 variants in the regulation of monocyte differentiation and eicosanoid metabolism, which could modify the immune response and promote inflammatory signaling within the local targeted organs and tissues including the kidney.

scholarly journals Inflammatory cell populations in early neuroinflammation in the core and peri-ischemic lesions of rat brain after transient focal cerebral ischemia: A morphometric study

2018 ◽  
Author(s):  
Emoke Horvath ◽  
Alex Oradan ◽  
Liviu Chiriac ◽  
Minodora Dobreanu ◽  
Előd-Ernő Nagy ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Rat Model ◽  
Inflammatory Cell ◽  
Focal Cerebral Ischemia ◽  
Artery Occlusion ◽  
The Core ◽  
Transient Focal Cerebral Ischemia ◽  
Cox 2 ◽  
Cerebral Artery Occlusion

Background and Objective: Clinical and experimental observations emphasize the role of inflammation as a direct risk factor for stroke. To better characterize the inflammation, we have conducted a detailed histological analysis of the inflammatory cell population after transient middle cerebral artery occlusion in a rat model. Methods: Fifteen adult Wistar male rats were divided randomly into test (n=10) and sham (n=5) groups. In the ischemic group, transient focal cerebral ischemia was induced with an intraluminal filament technique. Histologic lesions of the ischemic core and the surrounding penumbra zone were evaluated, based on a complex algorithm. Representative morphological changes in the core and the penumbra zone were compared. Immunohistochemistry was performed for leukocytes markers (CD15, CD68, CD3), leukocyte-released effectors (MMP-9 and COX-2), and FXIII (possibly involved in microglia and macrophage activation) Results: Neuronal vacuolation and degeneration were significantly more in the core lesion, whereas cellular edema and inflammatory infiltrate were increased in the penumbra. CD68, CD3, FXIII and Cox-2 expression were significantly higher in the penumbra than in the core (p=0.026; p=0.006; p=0.002; and p<0.001). Discussion: In the rat model of middle cerebral artery occlusion, inflammatory mechanisms, microglia/macrophage cells, and T-lymphocytes likely play an important role in the penumbra. The deterioration of neurons is less in the penumbra than in the core. Appreciation of the role of the inflammatory cells and mechanisms involved in stroke might lead to measures to inhibit the injury and save brain volume.

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