Gastroprotective effect of cilostazol against ethanol- and pylorus ligation–induced gastric lesions in rats
Despite the availability of effective antiulcer medications, their suboptimal safety profile ignites the search for alternative/complementary treatments. Drug repositioning is an attractive, efficient, and low-risk strategy. Cilostazol, a clinically used phosphodiesterase 3 inhibitor, has pronounced...
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| creator | Moawad, Helmy El Awdan, Sally A. Sallam, Nada A. El-Eraky, Wafaa I Alkhawlani, Mohammed A. |
| description | Despite the availability of effective antiulcer medications, their suboptimal safety profile ignites the search for alternative/complementary treatments. Drug repositioning is an attractive, efficient, and low-risk strategy. Cilostazol, a clinically used phosphodiesterase 3 inhibitor, has pronounced anti-inflammatory and vasodilatory effects suggesting antiulcer activity. Using ethanol-induced and pyloric ligation–induced gastric ulcer models, we investigated the gastroprotective effect of cilostazol (5 or 10 mg/kg, p.o.) in comparison with the standard antiulcer ranitidine (50 mg/kg, p.o.) in rats. Gastric mucosa was examined macroscopically, histologically, and biochemically for ulcer severity, markers of oxidative stress, proinflammatory cytokines, apoptotic, and cytoprotective mediators. Gastric acidic output, peptic activity, and mucin content were measured in gastric fluids. Pretreatment with cilostazol reduced ulcer number and severity, ameliorated redox status (reduced glutathione and malonaldehyde content), and decreased levels of IL-1β, IL-6, and TNF-훼 in gastric mucosa, in parallel with increases in mucosal defensive factors nitric oxide (NO), prostaglandin E
2
(PGE
2
), and heat-shock protein 70 (HSP70) promoting mucus secretion, tissue perfusion, and regeneration. Histological examination confirmed the beneficial effects of cilostazol in terms of reducing focal necrosis and infiltration of inflammatory cells, as well as increasing mucopolysaccharide content. These beneficial effects are likely secondary to an increase in cAMP and decrease in apoptosis regulator Bcl-2-associated X protein (BAX). Cilostazol, in a dose-dependent effect, exhibited vasodilatory, anti-inflammatory, and antiapoptotic actions in the gastric mucosa resulting in significant antiulcer activity comparable with the standard drug, ranitidine, but devoid of antisecretory activity. Therefore, its use should be dose and ulcer-inducer dependent. |
| doi_str_mv | 10.1007/s00210-019-01699-y |
| format | Article |
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2
(PGE
2
), and heat-shock protein 70 (HSP70) promoting mucus secretion, tissue perfusion, and regeneration. Histological examination confirmed the beneficial effects of cilostazol in terms of reducing focal necrosis and infiltration of inflammatory cells, as well as increasing mucopolysaccharide content. These beneficial effects are likely secondary to an increase in cAMP and decrease in apoptosis regulator Bcl-2-associated X protein (BAX). Cilostazol, in a dose-dependent effect, exhibited vasodilatory, anti-inflammatory, and antiapoptotic actions in the gastric mucosa resulting in significant antiulcer activity comparable with the standard drug, ranitidine, but devoid of antisecretory activity. Therefore, its use should be dose and ulcer-inducer dependent.</description><identifier>ISSN: 0028-1298</identifier><identifier>EISSN: 1432-1912</identifier><identifier>DOI: 10.1007/s00210-019-01699-y</identifier><identifier>PMID: 31372695</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer Berlin Heidelberg</publisher><subject>Acidic oxides ; Animals ; Anti-Ulcer Agents - pharmacology ; Anti-Ulcer Agents - therapeutic use ; Apoptosis ; BAX protein ; Bcl-2 protein ; Bcl-x protein ; Biomedical and Life Sciences ; Biomedicine ; Cilostazol - pharmacology ; Cilostazol - therapeutic use ; Computational fluid dynamics ; Cytokines - metabolism ; Dinoprostone - metabolism ; Drug dosages ; Ethanol ; Gastric juice ; Gastric mucosa ; Gastric Mucosa - drug effects ; Gastric Mucosa - metabolism ; Gastric Mucosa - pathology ; Glutathione ; HSP70 Heat-Shock Proteins - metabolism ; Hsp70 protein ; IL-1β ; Inflammation ; Interleukin 6 ; Lesions ; Male ; Malondialdehyde ; Mucin ; Mucus ; Neurosciences ; Nitric oxide ; Nitric Oxide - metabolism ; Original Article ; Oxidative stress ; Perfusion ; Pharmacology/Toxicology ; Phosphodiesterase ; Prostaglandin E2 ; Pylorus - surgery ; Ranitidine ; Rats, Wistar ; Stomach Ulcer - drug therapy ; Stomach Ulcer - etiology ; Stomach Ulcer - metabolism ; Stomach Ulcer - pathology ; Tumor necrosis factor ; Ulcers</subject><ispartof>Naunyn-Schmiedeberg's archives of pharmacology, 2019-12, Vol.392 (12), p.1605-1616</ispartof><rights>Springer-Verlag GmbH Germany, part of Springer Nature 2019</rights><rights>Naunyn-Schmiedeberg's Archives of Pharmacology is a copyright of Springer, (2019). All Rights Reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c375t-91d8f827293d87f33d3434397ba18d48b84247695e95b0898789d55934e8538d3</citedby><cites>FETCH-LOGICAL-c375t-91d8f827293d87f33d3434397ba18d48b84247695e95b0898789d55934e8538d3</cites><orcidid>0000-0002-0673-2347</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00210-019-01699-y$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00210-019-01699-y$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27903,27904,41467,42536,51297</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31372695$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Moawad, Helmy</creatorcontrib><creatorcontrib>El Awdan, Sally A.</creatorcontrib><creatorcontrib>Sallam, Nada A.</creatorcontrib><creatorcontrib>El-Eraky, Wafaa I</creatorcontrib><creatorcontrib>Alkhawlani, Mohammed A.</creatorcontrib><title>Gastroprotective effect of cilostazol against ethanol- and pylorus ligation–induced gastric lesions in rats</title><title>Naunyn-Schmiedeberg's archives of pharmacology</title><addtitle>Naunyn-Schmiedeberg's Arch Pharmacol</addtitle><addtitle>Naunyn Schmiedebergs Arch Pharmacol</addtitle><description>Despite the availability of effective antiulcer medications, their suboptimal safety profile ignites the search for alternative/complementary treatments. Drug repositioning is an attractive, efficient, and low-risk strategy. Cilostazol, a clinically used phosphodiesterase 3 inhibitor, has pronounced anti-inflammatory and vasodilatory effects suggesting antiulcer activity. Using ethanol-induced and pyloric ligation–induced gastric ulcer models, we investigated the gastroprotective effect of cilostazol (5 or 10 mg/kg, p.o.) in comparison with the standard antiulcer ranitidine (50 mg/kg, p.o.) in rats. Gastric mucosa was examined macroscopically, histologically, and biochemically for ulcer severity, markers of oxidative stress, proinflammatory cytokines, apoptotic, and cytoprotective mediators. Gastric acidic output, peptic activity, and mucin content were measured in gastric fluids. Pretreatment with cilostazol reduced ulcer number and severity, ameliorated redox status (reduced glutathione and malonaldehyde content), and decreased levels of IL-1β, IL-6, and TNF-훼 in gastric mucosa, in parallel with increases in mucosal defensive factors nitric oxide (NO), prostaglandin E
2
(PGE
2
), and heat-shock protein 70 (HSP70) promoting mucus secretion, tissue perfusion, and regeneration. Histological examination confirmed the beneficial effects of cilostazol in terms of reducing focal necrosis and infiltration of inflammatory cells, as well as increasing mucopolysaccharide content. These beneficial effects are likely secondary to an increase in cAMP and decrease in apoptosis regulator Bcl-2-associated X protein (BAX). Cilostazol, in a dose-dependent effect, exhibited vasodilatory, anti-inflammatory, and antiapoptotic actions in the gastric mucosa resulting in significant antiulcer activity comparable with the standard drug, ranitidine, but devoid of antisecretory activity. Therefore, its use should be dose and ulcer-inducer dependent.</description><subject>Acidic oxides</subject><subject>Animals</subject><subject>Anti-Ulcer Agents - pharmacology</subject><subject>Anti-Ulcer Agents - therapeutic use</subject><subject>Apoptosis</subject><subject>BAX protein</subject><subject>Bcl-2 protein</subject><subject>Bcl-x protein</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cilostazol - pharmacology</subject><subject>Cilostazol - therapeutic use</subject><subject>Computational fluid dynamics</subject><subject>Cytokines - metabolism</subject><subject>Dinoprostone - metabolism</subject><subject>Drug dosages</subject><subject>Ethanol</subject><subject>Gastric juice</subject><subject>Gastric mucosa</subject><subject>Gastric Mucosa - drug effects</subject><subject>Gastric Mucosa - metabolism</subject><subject>Gastric Mucosa - pathology</subject><subject>Glutathione</subject><subject>HSP70 Heat-Shock Proteins - metabolism</subject><subject>Hsp70 protein</subject><subject>IL-1β</subject><subject>Inflammation</subject><subject>Interleukin 6</subject><subject>Lesions</subject><subject>Male</subject><subject>Malondialdehyde</subject><subject>Mucin</subject><subject>Mucus</subject><subject>Neurosciences</subject><subject>Nitric oxide</subject><subject>Nitric Oxide - metabolism</subject><subject>Original Article</subject><subject>Oxidative stress</subject><subject>Perfusion</subject><subject>Pharmacology/Toxicology</subject><subject>Phosphodiesterase</subject><subject>Prostaglandin E2</subject><subject>Pylorus - surgery</subject><subject>Ranitidine</subject><subject>Rats, Wistar</subject><subject>Stomach Ulcer - drug therapy</subject><subject>Stomach Ulcer - etiology</subject><subject>Stomach Ulcer - metabolism</subject><subject>Stomach Ulcer - pathology</subject><subject>Tumor necrosis factor</subject><subject>Ulcers</subject><issn>0028-1298</issn><issn>1432-1912</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNp9kM1KAzEUhYMotlZfwIUEXI_mZ9IkSylaBcGNrkNmkhlTppOaZIS68h18Q5_E1FbdSbgkcM49N_cD4BSjC4wQv4wIEYwKhGWuqZTFeg-McUlJgSUm-2CcdVFgIsUIHMW4QAhNMWOHYEQx5WQq2Rgs5zqm4FfBJ1sn92qhbZr8gr6Btet8TPrNd1C32vUxQZuede-7AurewNW682GIsHOtTs73n-8frjdDbQ1sN6muhp2NWYjQ9TDoFI_BQaO7aE929wQ83Vw_zm6L-4f53ezqvqgpZ6mQ2IhGEE4kNYI3lBpa5iN5pbEwpahESUqe_28lq5CQggtpGJO0tIJRYegEnG9z814vg41JLfwQ-jxSETLljEvKaHaRrasOPsZgG7UKbqnDWmGkNoTVlrDKhNU3YbXOTWe76KFaWvPb8oM0G-jWELPUtzb8zf4n9guT5Ihw</recordid><startdate>20191201</startdate><enddate>20191201</enddate><creator>Moawad, Helmy</creator><creator>El Awdan, Sally A.</creator><creator>Sallam, Nada A.</creator><creator>El-Eraky, Wafaa I</creator><creator>Alkhawlani, Mohammed A.</creator><general>Springer Berlin Heidelberg</general><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QP</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><orcidid>https://orcid.org/0000-0002-0673-2347</orcidid></search><sort><creationdate>20191201</creationdate><title>Gastroprotective effect of cilostazol against ethanol- and pylorus ligation–induced gastric lesions in rats</title><author>Moawad, Helmy ; El Awdan, Sally A. ; Sallam, Nada A. ; El-Eraky, Wafaa I ; Alkhawlani, Mohammed A.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c375t-91d8f827293d87f33d3434397ba18d48b84247695e95b0898789d55934e8538d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Acidic oxides</topic><topic>Animals</topic><topic>Anti-Ulcer Agents - pharmacology</topic><topic>Anti-Ulcer Agents - therapeutic use</topic><topic>Apoptosis</topic><topic>BAX protein</topic><topic>Bcl-2 protein</topic><topic>Bcl-x protein</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Cilostazol - pharmacology</topic><topic>Cilostazol - therapeutic use</topic><topic>Computational fluid dynamics</topic><topic>Cytokines - metabolism</topic><topic>Dinoprostone - metabolism</topic><topic>Drug dosages</topic><topic>Ethanol</topic><topic>Gastric juice</topic><topic>Gastric mucosa</topic><topic>Gastric Mucosa - drug effects</topic><topic>Gastric Mucosa - metabolism</topic><topic>Gastric Mucosa - pathology</topic><topic>Glutathione</topic><topic>HSP70 Heat-Shock Proteins - metabolism</topic><topic>Hsp70 protein</topic><topic>IL-1β</topic><topic>Inflammation</topic><topic>Interleukin 6</topic><topic>Lesions</topic><topic>Male</topic><topic>Malondialdehyde</topic><topic>Mucin</topic><topic>Mucus</topic><topic>Neurosciences</topic><topic>Nitric oxide</topic><topic>Nitric Oxide - metabolism</topic><topic>Original Article</topic><topic>Oxidative stress</topic><topic>Perfusion</topic><topic>Pharmacology/Toxicology</topic><topic>Phosphodiesterase</topic><topic>Prostaglandin E2</topic><topic>Pylorus - surgery</topic><topic>Ranitidine</topic><topic>Rats, Wistar</topic><topic>Stomach Ulcer - drug therapy</topic><topic>Stomach Ulcer - etiology</topic><topic>Stomach Ulcer - metabolism</topic><topic>Stomach Ulcer - pathology</topic><topic>Tumor necrosis factor</topic><topic>Ulcers</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Moawad, Helmy</creatorcontrib><creatorcontrib>El Awdan, Sally A.</creatorcontrib><creatorcontrib>Sallam, Nada A.</creatorcontrib><creatorcontrib>El-Eraky, Wafaa I</creatorcontrib><creatorcontrib>Alkhawlani, Mohammed A.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><jtitle>Naunyn-Schmiedeberg's archives of pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Moawad, Helmy</au><au>El Awdan, Sally A.</au><au>Sallam, Nada A.</au><au>El-Eraky, Wafaa I</au><au>Alkhawlani, Mohammed A.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Gastroprotective effect of cilostazol against ethanol- and pylorus ligation–induced gastric lesions in rats</atitle><jtitle>Naunyn-Schmiedeberg's archives of pharmacology</jtitle><stitle>Naunyn-Schmiedeberg's Arch Pharmacol</stitle><addtitle>Naunyn Schmiedebergs Arch Pharmacol</addtitle><date>2019-12-01</date><risdate>2019</risdate><volume>392</volume><issue>12</issue><spage>1605</spage><epage>1616</epage><pages>1605-1616</pages><issn>0028-1298</issn><eissn>1432-1912</eissn><abstract>Despite the availability of effective antiulcer medications, their suboptimal safety profile ignites the search for alternative/complementary treatments. Drug repositioning is an attractive, efficient, and low-risk strategy. Cilostazol, a clinically used phosphodiesterase 3 inhibitor, has pronounced anti-inflammatory and vasodilatory effects suggesting antiulcer activity. Using ethanol-induced and pyloric ligation–induced gastric ulcer models, we investigated the gastroprotective effect of cilostazol (5 or 10 mg/kg, p.o.) in comparison with the standard antiulcer ranitidine (50 mg/kg, p.o.) in rats. Gastric mucosa was examined macroscopically, histologically, and biochemically for ulcer severity, markers of oxidative stress, proinflammatory cytokines, apoptotic, and cytoprotective mediators. Gastric acidic output, peptic activity, and mucin content were measured in gastric fluids. Pretreatment with cilostazol reduced ulcer number and severity, ameliorated redox status (reduced glutathione and malonaldehyde content), and decreased levels of IL-1β, IL-6, and TNF-훼 in gastric mucosa, in parallel with increases in mucosal defensive factors nitric oxide (NO), prostaglandin E
2
(PGE
2
), and heat-shock protein 70 (HSP70) promoting mucus secretion, tissue perfusion, and regeneration. Histological examination confirmed the beneficial effects of cilostazol in terms of reducing focal necrosis and infiltration of inflammatory cells, as well as increasing mucopolysaccharide content. These beneficial effects are likely secondary to an increase in cAMP and decrease in apoptosis regulator Bcl-2-associated X protein (BAX). Cilostazol, in a dose-dependent effect, exhibited vasodilatory, anti-inflammatory, and antiapoptotic actions in the gastric mucosa resulting in significant antiulcer activity comparable with the standard drug, ranitidine, but devoid of antisecretory activity. Therefore, its use should be dose and ulcer-inducer dependent.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer Berlin Heidelberg</pub><pmid>31372695</pmid><doi>10.1007/s00210-019-01699-y</doi><tpages>12</tpages><orcidid>https://orcid.org/0000-0002-0673-2347</orcidid></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0028-1298 |
| ispartof | Naunyn-Schmiedeberg's archives of pharmacology, 2019-12, Vol.392 (12), p.1605-1616 |
| issn | 0028-1298 1432-1912 |
| language | eng |
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| subjects | Acidic oxides Animals Anti-Ulcer Agents - pharmacology Anti-Ulcer Agents - therapeutic use Apoptosis BAX protein Bcl-2 protein Bcl-x protein Biomedical and Life Sciences Biomedicine Cilostazol - pharmacology Cilostazol - therapeutic use Computational fluid dynamics Cytokines - metabolism Dinoprostone - metabolism Drug dosages Ethanol Gastric juice Gastric mucosa Gastric Mucosa - drug effects Gastric Mucosa - metabolism Gastric Mucosa - pathology Glutathione HSP70 Heat-Shock Proteins - metabolism Hsp70 protein IL-1β Inflammation Interleukin 6 Lesions Male Malondialdehyde Mucin Mucus Neurosciences Nitric oxide Nitric Oxide - metabolism Original Article Oxidative stress Perfusion Pharmacology/Toxicology Phosphodiesterase Prostaglandin E2 Pylorus - surgery Ranitidine Rats, Wistar Stomach Ulcer - drug therapy Stomach Ulcer - etiology Stomach Ulcer - metabolism Stomach Ulcer - pathology Tumor necrosis factor Ulcers |
| title | Gastroprotective effect of cilostazol against ethanol- and pylorus ligation–induced gastric lesions in rats |
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