Montelukast potentiates the antiinflammatory effect of NSAIDs in the rat paw formalin model and simultaneously minimizes the risk of gastric damage

Objective and design Montelukast, a cysteinyl leukotriene receptor antagonist, exhibits antiinflammatory action. We tested whether exposure to montelukast plus nonsteroidal antiinflammatory drugs (NSAIDs) elicits better control of paw inflammation in the rat formalin test and improves associated gas...

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Veröffentlicht in:Inflammation research 2021-09, Vol.70 (9), p.981-992
Hauptverfasser: Abdelhady, Sherien A., Ali, Mennatallah A., Al-Shafie, Tamer A., Abdelmawgoud, Ebtsam M., Yacout, Dalia M., El-Mas, Mahmoud M.
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container_end_page 992
container_issue 9
container_start_page 981
container_title Inflammation research
container_volume 70
creator Abdelhady, Sherien A.
Ali, Mennatallah A.
Al-Shafie, Tamer A.
Abdelmawgoud, Ebtsam M.
Yacout, Dalia M.
El-Mas, Mahmoud M.
description Objective and design Montelukast, a cysteinyl leukotriene receptor antagonist, exhibits antiinflammatory action. We tested whether exposure to montelukast plus nonsteroidal antiinflammatory drugs (NSAIDs) elicits better control of paw inflammation in the rat formalin test and improves associated gastric damage. Materials A total of 46 adult male rats were used in the study. Treatments We evaluated separate and combined effects of montelukast (20 mg/kg), celecoxib (COX2 inhibitor, 10 mg/kg), and diclofenac (nonselective COX1/COX2 inhibitor, 10 mg/kg) on paw and gastric damage in the rat formalin test. Results Individual pretreatments of rats with montelukast, diclofenac, or celecoxib partly reduced formalin-induced increases in (i) paw edema, fibrosis, and inflammatory cells, (iii) serum interleukin-6 (IL-6) and leukotrienes (LTB4 and LTD4), and (iv) paw expressions of inducible nitric oxide synthase (iNOS) and COX2. These effects were accentuated in rats treated with montelukast plus diclofenac or montelukast plus celecoxib. Alternatively, montelukast or celecoxib, but not diclofenac, alleviated formalin-evoked gastric damage and increments in tumor necrosis factor-α and decrements in prostaglandin-E 2 . These advantageous gastric influences were potentiated in rats treated with montelukast plus celecoxib. Conclusions While montelukast equally enhances antiinflammatory action of diclofenac or celecoxib via downregulating iNOS/COX2/LTs/IL-6 signaling, its gastroprotective action is preferentially potentiated by celecoxib.
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We tested whether exposure to montelukast plus nonsteroidal antiinflammatory drugs (NSAIDs) elicits better control of paw inflammation in the rat formalin test and improves associated gastric damage. Materials A total of 46 adult male rats were used in the study. Treatments We evaluated separate and combined effects of montelukast (20 mg/kg), celecoxib (COX2 inhibitor, 10 mg/kg), and diclofenac (nonselective COX1/COX2 inhibitor, 10 mg/kg) on paw and gastric damage in the rat formalin test. Results Individual pretreatments of rats with montelukast, diclofenac, or celecoxib partly reduced formalin-induced increases in (i) paw edema, fibrosis, and inflammatory cells, (iii) serum interleukin-6 (IL-6) and leukotrienes (LTB4 and LTD4), and (iv) paw expressions of inducible nitric oxide synthase (iNOS) and COX2. These effects were accentuated in rats treated with montelukast plus diclofenac or montelukast plus celecoxib. Alternatively, montelukast or celecoxib, but not diclofenac, alleviated formalin-evoked gastric damage and increments in tumor necrosis factor-α and decrements in prostaglandin-E 2 . These advantageous gastric influences were potentiated in rats treated with montelukast plus celecoxib. Conclusions While montelukast equally enhances antiinflammatory action of diclofenac or celecoxib via downregulating iNOS/COX2/LTs/IL-6 signaling, its gastroprotective action is preferentially potentiated by celecoxib.</description><identifier>ISSN: 1023-3830</identifier><identifier>EISSN: 1420-908X</identifier><identifier>DOI: 10.1007/s00011-021-01492-9</identifier><identifier>PMID: 34382102</identifier><language>eng</language><publisher>Cham: Springer International Publishing</publisher><subject><![CDATA[Acetates - administration & dosage ; Allergology ; Animals ; Anti-inflammatory agents ; Anti-Inflammatory Agents, Non-Steroidal - administration & dosage ; Biomedical and Life Sciences ; Biomedicine ; Celecoxib ; Celecoxib - administration & dosage ; COX-2 inhibitors ; Cyclooxygenase 2 - metabolism ; Cyclooxygenase-2 ; Cyclopropanes - administration & dosage ; Damage ; Dermatology ; Diclofenac ; Diclofenac - administration & dosage ; Edema ; Fibrosis ; Formaldehyde ; Formaldehyde - chemistry ; Immunology ; Inflammation ; Inflammation - drug therapy ; Interleukin 6 ; Leukotrienes ; Male ; Montelukast ; Neurology ; Nitric oxide ; Nitric Oxide Synthase Type II - metabolism ; Nitric-oxide synthase ; Nonsteroidal anti-inflammatory drugs ; Original Research Paper ; Pain perception ; Pharmacology/Toxicology ; Quinolines - administration & dosage ; Rats ; Rats, Wistar ; Rheumatology ; Risk ; Rodents ; Signal Transduction ; Stomach - drug effects ; Sulfides - administration & dosage ; Tumor necrosis factor-α]]></subject><ispartof>Inflammation research, 2021-09, Vol.70 (9), p.981-992</ispartof><rights>The Author(s), under exclusive licence to Springer Nature Switzerland AG 2021</rights><rights>2021. 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Res</addtitle><addtitle>Inflamm Res</addtitle><description>Objective and design Montelukast, a cysteinyl leukotriene receptor antagonist, exhibits antiinflammatory action. We tested whether exposure to montelukast plus nonsteroidal antiinflammatory drugs (NSAIDs) elicits better control of paw inflammation in the rat formalin test and improves associated gastric damage. Materials A total of 46 adult male rats were used in the study. Treatments We evaluated separate and combined effects of montelukast (20 mg/kg), celecoxib (COX2 inhibitor, 10 mg/kg), and diclofenac (nonselective COX1/COX2 inhibitor, 10 mg/kg) on paw and gastric damage in the rat formalin test. Results Individual pretreatments of rats with montelukast, diclofenac, or celecoxib partly reduced formalin-induced increases in (i) paw edema, fibrosis, and inflammatory cells, (iii) serum interleukin-6 (IL-6) and leukotrienes (LTB4 and LTD4), and (iv) paw expressions of inducible nitric oxide synthase (iNOS) and COX2. These effects were accentuated in rats treated with montelukast plus diclofenac or montelukast plus celecoxib. Alternatively, montelukast or celecoxib, but not diclofenac, alleviated formalin-evoked gastric damage and increments in tumor necrosis factor-α and decrements in prostaglandin-E 2 . These advantageous gastric influences were potentiated in rats treated with montelukast plus celecoxib. Conclusions While montelukast equally enhances antiinflammatory action of diclofenac or celecoxib via downregulating iNOS/COX2/LTs/IL-6 signaling, its gastroprotective action is preferentially potentiated by celecoxib.</description><subject>Acetates - administration &amp; dosage</subject><subject>Allergology</subject><subject>Animals</subject><subject>Anti-inflammatory agents</subject><subject>Anti-Inflammatory Agents, Non-Steroidal - administration &amp; dosage</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Celecoxib</subject><subject>Celecoxib - administration &amp; dosage</subject><subject>COX-2 inhibitors</subject><subject>Cyclooxygenase 2 - metabolism</subject><subject>Cyclooxygenase-2</subject><subject>Cyclopropanes - administration &amp; dosage</subject><subject>Damage</subject><subject>Dermatology</subject><subject>Diclofenac</subject><subject>Diclofenac - administration &amp; dosage</subject><subject>Edema</subject><subject>Fibrosis</subject><subject>Formaldehyde</subject><subject>Formaldehyde - chemistry</subject><subject>Immunology</subject><subject>Inflammation</subject><subject>Inflammation - drug therapy</subject><subject>Interleukin 6</subject><subject>Leukotrienes</subject><subject>Male</subject><subject>Montelukast</subject><subject>Neurology</subject><subject>Nitric oxide</subject><subject>Nitric Oxide Synthase Type II - metabolism</subject><subject>Nitric-oxide synthase</subject><subject>Nonsteroidal anti-inflammatory drugs</subject><subject>Original Research Paper</subject><subject>Pain perception</subject><subject>Pharmacology/Toxicology</subject><subject>Quinolines - administration &amp; 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Res</stitle><addtitle>Inflamm Res</addtitle><date>2021-09-01</date><risdate>2021</risdate><volume>70</volume><issue>9</issue><spage>981</spage><epage>992</epage><pages>981-992</pages><issn>1023-3830</issn><eissn>1420-908X</eissn><abstract>Objective and design Montelukast, a cysteinyl leukotriene receptor antagonist, exhibits antiinflammatory action. We tested whether exposure to montelukast plus nonsteroidal antiinflammatory drugs (NSAIDs) elicits better control of paw inflammation in the rat formalin test and improves associated gastric damage. Materials A total of 46 adult male rats were used in the study. Treatments We evaluated separate and combined effects of montelukast (20 mg/kg), celecoxib (COX2 inhibitor, 10 mg/kg), and diclofenac (nonselective COX1/COX2 inhibitor, 10 mg/kg) on paw and gastric damage in the rat formalin test. Results Individual pretreatments of rats with montelukast, diclofenac, or celecoxib partly reduced formalin-induced increases in (i) paw edema, fibrosis, and inflammatory cells, (iii) serum interleukin-6 (IL-6) and leukotrienes (LTB4 and LTD4), and (iv) paw expressions of inducible nitric oxide synthase (iNOS) and COX2. These effects were accentuated in rats treated with montelukast plus diclofenac or montelukast plus celecoxib. Alternatively, montelukast or celecoxib, but not diclofenac, alleviated formalin-evoked gastric damage and increments in tumor necrosis factor-α and decrements in prostaglandin-E 2 . These advantageous gastric influences were potentiated in rats treated with montelukast plus celecoxib. Conclusions While montelukast equally enhances antiinflammatory action of diclofenac or celecoxib via downregulating iNOS/COX2/LTs/IL-6 signaling, its gastroprotective action is preferentially potentiated by celecoxib.</abstract><cop>Cham</cop><pub>Springer International Publishing</pub><pmid>34382102</pmid><doi>10.1007/s00011-021-01492-9</doi><tpages>12</tpages><orcidid>https://orcid.org/0000-0001-8855-7070</orcidid></addata></record>
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subjects Acetates - administration & dosage
Allergology
Animals
Anti-inflammatory agents
Anti-Inflammatory Agents, Non-Steroidal - administration & dosage
Biomedical and Life Sciences
Biomedicine
Celecoxib
Celecoxib - administration & dosage
COX-2 inhibitors
Cyclooxygenase 2 - metabolism
Cyclooxygenase-2
Cyclopropanes - administration & dosage
Damage
Dermatology
Diclofenac
Diclofenac - administration & dosage
Edema
Fibrosis
Formaldehyde
Formaldehyde - chemistry
Immunology
Inflammation
Inflammation - drug therapy
Interleukin 6
Leukotrienes
Male
Montelukast
Neurology
Nitric oxide
Nitric Oxide Synthase Type II - metabolism
Nitric-oxide synthase
Nonsteroidal anti-inflammatory drugs
Original Research Paper
Pain perception
Pharmacology/Toxicology
Quinolines - administration & dosage
Rats
Rats, Wistar
Rheumatology
Risk
Rodents
Signal Transduction
Stomach - drug effects
Sulfides - administration & dosage
Tumor necrosis factor-α
title Montelukast potentiates the antiinflammatory effect of NSAIDs in the rat paw formalin model and simultaneously minimizes the risk of gastric damage
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