Antioxidant, Anti-inflammatory, and Antiulcer Potential of Manuka Honey against Gastric Ulcer in Rats
Gastric ulcers are among the most common diseases affecting humans. This study aimed at investigating the gastroprotective effects of manuka honey against ethanol-induced gastric ulcers in rats. The mechanism by which honey exerts its antiulcer potential was elucidated. Four groups of rats were used...
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| Veröffentlicht in: | Oxidative medicine and cellular longevity 2016-01, Vol.2016 (2016), p.1-10 |
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| description | Gastric ulcers are among the most common diseases affecting humans. This study aimed at investigating the gastroprotective effects of manuka honey against ethanol-induced gastric ulcers in rats. The mechanism by which honey exerts its antiulcer potential was elucidated. Four groups of rats were used: control, ethanol (ulcer), omeprazole, and manuka honey. Stomachs were examined macroscopically for hemorrhagic lesions in the glandular mucosa, histopathological changes, and glycoprotein detection. The effects of oxidative stress were investigated using the following indicators: gastric mucosal nitric oxide (NO), reduced glutathione (GSH), lipid peroxide (MDA, measured as malondialdehyde) glutathione peroxidase (GPx), superoxide dismutase (SOD), and catalase. Plasma tumour necrosis factor-α, interleukin-1β, and IL-6 were also measured. Manuka honey significantly decreased the ulcer index, completely protected the mucosa from lesions, and preserved gastric mucosal glycoprotein. It significantly increased gastric mucosal levels of NO, GSH, GPx, and SOD. Manuka honey also decreased gastric mucosal MDA and plasma TNF-α, IL-1β, and IL-6 concentrations. In conclusion, manuka honey likely exerted its antiulcer, effect by keeping enzymatic (GPx and SOD) and nonenzymatic (GSH and NO) antioxidants as well as inflammatory cytokines (TNF-α, IL-1β, and IL-6) in a reduced form, inhibited lipid peroxidation (MDA), and preserved mucous glycoproteins levels. |
| doi_str_mv | 10.1155/2016/3643824 |
| format | Article |
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This study aimed at investigating the gastroprotective effects of manuka honey against ethanol-induced gastric ulcers in rats. The mechanism by which honey exerts its antiulcer potential was elucidated. Four groups of rats were used: control, ethanol (ulcer), omeprazole, and manuka honey. Stomachs were examined macroscopically for hemorrhagic lesions in the glandular mucosa, histopathological changes, and glycoprotein detection. The effects of oxidative stress were investigated using the following indicators: gastric mucosal nitric oxide (NO), reduced glutathione (GSH), lipid peroxide (MDA, measured as malondialdehyde) glutathione peroxidase (GPx), superoxide dismutase (SOD), and catalase. Plasma tumour necrosis factor-α, interleukin-1β, and IL-6 were also measured. Manuka honey significantly decreased the ulcer index, completely protected the mucosa from lesions, and preserved gastric mucosal glycoprotein. It significantly increased gastric mucosal levels of NO, GSH, GPx, and SOD. Manuka honey also decreased gastric mucosal MDA and plasma TNF-α, IL-1β, and IL-6 concentrations. In conclusion, manuka honey likely exerted its antiulcer, effect by keeping enzymatic (GPx and SOD) and nonenzymatic (GSH and NO) antioxidants as well as inflammatory cytokines (TNF-α, IL-1β, and IL-6) in a reduced form, inhibited lipid peroxidation (MDA), and preserved mucous glycoproteins levels.</description><identifier>ISSN: 1942-0900</identifier><identifier>EISSN: 1942-0994</identifier><identifier>DOI: 10.1155/2016/3643824</identifier><identifier>PMID: 26770649</identifier><language>eng</language><publisher>Cairo, Egypt: Hindawi Publishing Corporation</publisher><subject>Animals ; Anti-Inflammatory Agents - pharmacology ; Anti-Inflammatory Agents - therapeutic use ; Anti-inflammatory drugs ; Antioxidants ; Antioxidants - pharmacology ; Antioxidants - therapeutic use ; Blood Glucose - metabolism ; Catalase - metabolism ; Cholesterol - blood ; Cytokines ; Disease Models, Animal ; Drinking Behavior - drug effects ; Drug dosages ; Enzymes ; Ethanol ; Feeding Behavior - drug effects ; Flavonoids ; Glutathione - metabolism ; Glutathione Peroxidase - metabolism ; Glycoproteins - metabolism ; Honey ; Interleukin-1beta - blood ; Interleukin-6 - blood ; Interleukins ; Lipid peroxidation ; Lipids ; Male ; Malondialdehyde - metabolism ; Medical research ; Nitric oxide ; Nitric Oxide - metabolism ; Omeprazole ; Rats ; Research centers ; Rodents ; Staining and Labeling ; Stomach Ulcer - drug therapy ; Stomach Ulcer - pathology ; Studies ; Superoxide ; Superoxide Dismutase - metabolism ; Toxicology ; Triglycerides - blood ; Tumor Necrosis Factor-alpha - blood ; Tumor necrosis factor-TNF ; Ulcers ; Weight Gain - drug effects</subject><ispartof>Oxidative medicine and cellular longevity, 2016-01, Vol.2016 (2016), p.1-10</ispartof><rights>Copyright © 2016 Saad B. Almasaudi et al.</rights><rights>COPYRIGHT 2015 John Wiley & Sons, Inc.</rights><rights>Copyright © 2016 Saad B. Almasaudi et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.</rights><rights>Copyright © 2016 Saad B. Almasaudi et al. 2016</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c565t-52b7fba0ad291563cf3576d10fe7b9b5f86b1f29b9ae670cbb5ad86d811fca4d3</citedby><cites>FETCH-LOGICAL-c565t-52b7fba0ad291563cf3576d10fe7b9b5f86b1f29b9ae670cbb5ad86d811fca4d3</cites><orcidid>0000-0001-7512-8787</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4685122/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4685122/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26770649$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Noguchi, Noriko</contributor><creatorcontrib>Harakeh, Steve</creatorcontrib><creatorcontrib>Ali, Soad S.</creatorcontrib><creatorcontrib>Abdel-dayem, Umama A.</creatorcontrib><creatorcontrib>Abbas, Aymn T.</creatorcontrib><creatorcontrib>El-Shitany, Nagla A.</creatorcontrib><creatorcontrib>Almasaudi, Saad B.</creatorcontrib><creatorcontrib>Al Jaouni, Soad K.</creatorcontrib><title>Antioxidant, Anti-inflammatory, and Antiulcer Potential of Manuka Honey against Gastric Ulcer in Rats</title><title>Oxidative medicine and cellular longevity</title><addtitle>Oxid Med Cell Longev</addtitle><description>Gastric ulcers are among the most common diseases affecting humans. This study aimed at investigating the gastroprotective effects of manuka honey against ethanol-induced gastric ulcers in rats. The mechanism by which honey exerts its antiulcer potential was elucidated. Four groups of rats were used: control, ethanol (ulcer), omeprazole, and manuka honey. Stomachs were examined macroscopically for hemorrhagic lesions in the glandular mucosa, histopathological changes, and glycoprotein detection. The effects of oxidative stress were investigated using the following indicators: gastric mucosal nitric oxide (NO), reduced glutathione (GSH), lipid peroxide (MDA, measured as malondialdehyde) glutathione peroxidase (GPx), superoxide dismutase (SOD), and catalase. Plasma tumour necrosis factor-α, interleukin-1β, and IL-6 were also measured. Manuka honey significantly decreased the ulcer index, completely protected the mucosa from lesions, and preserved gastric mucosal glycoprotein. It significantly increased gastric mucosal levels of NO, GSH, GPx, and SOD. Manuka honey also decreased gastric mucosal MDA and plasma TNF-α, IL-1β, and IL-6 concentrations. In conclusion, manuka honey likely exerted its antiulcer, effect by keeping enzymatic (GPx and SOD) and nonenzymatic (GSH and NO) antioxidants as well as inflammatory cytokines (TNF-α, IL-1β, and IL-6) in a reduced form, inhibited lipid peroxidation (MDA), and preserved mucous glycoproteins levels.</description><subject>Animals</subject><subject>Anti-Inflammatory Agents - pharmacology</subject><subject>Anti-Inflammatory Agents - therapeutic use</subject><subject>Anti-inflammatory drugs</subject><subject>Antioxidants</subject><subject>Antioxidants - pharmacology</subject><subject>Antioxidants - therapeutic use</subject><subject>Blood Glucose - metabolism</subject><subject>Catalase - metabolism</subject><subject>Cholesterol - blood</subject><subject>Cytokines</subject><subject>Disease Models, Animal</subject><subject>Drinking Behavior - drug effects</subject><subject>Drug dosages</subject><subject>Enzymes</subject><subject>Ethanol</subject><subject>Feeding Behavior - drug effects</subject><subject>Flavonoids</subject><subject>Glutathione - metabolism</subject><subject>Glutathione Peroxidase - metabolism</subject><subject>Glycoproteins - metabolism</subject><subject>Honey</subject><subject>Interleukin-1beta - blood</subject><subject>Interleukin-6 - blood</subject><subject>Interleukins</subject><subject>Lipid peroxidation</subject><subject>Lipids</subject><subject>Male</subject><subject>Malondialdehyde - metabolism</subject><subject>Medical research</subject><subject>Nitric oxide</subject><subject>Nitric Oxide - metabolism</subject><subject>Omeprazole</subject><subject>Rats</subject><subject>Research centers</subject><subject>Rodents</subject><subject>Staining and Labeling</subject><subject>Stomach Ulcer - drug therapy</subject><subject>Stomach Ulcer - pathology</subject><subject>Studies</subject><subject>Superoxide</subject><subject>Superoxide Dismutase - metabolism</subject><subject>Toxicology</subject><subject>Triglycerides - blood</subject><subject>Tumor Necrosis Factor-alpha - blood</subject><subject>Tumor necrosis factor-TNF</subject><subject>Ulcers</subject><subject>Weight Gain - 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metabolism</topic><topic>Omeprazole</topic><topic>Rats</topic><topic>Research centers</topic><topic>Rodents</topic><topic>Staining and Labeling</topic><topic>Stomach Ulcer - drug therapy</topic><topic>Stomach Ulcer - pathology</topic><topic>Studies</topic><topic>Superoxide</topic><topic>Superoxide Dismutase - metabolism</topic><topic>Toxicology</topic><topic>Triglycerides - blood</topic><topic>Tumor Necrosis Factor-alpha - blood</topic><topic>Tumor necrosis factor-TNF</topic><topic>Ulcers</topic><topic>Weight Gain - drug effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Harakeh, Steve</creatorcontrib><creatorcontrib>Ali, Soad S.</creatorcontrib><creatorcontrib>Abdel-dayem, Umama A.</creatorcontrib><creatorcontrib>Abbas, Aymn T.</creatorcontrib><creatorcontrib>El-Shitany, Nagla A.</creatorcontrib><creatorcontrib>Almasaudi, Saad B.</creatorcontrib><creatorcontrib>Al Jaouni, Soad K.</creatorcontrib><collection>الدوريات العلمية والإحصائية - 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This study aimed at investigating the gastroprotective effects of manuka honey against ethanol-induced gastric ulcers in rats. The mechanism by which honey exerts its antiulcer potential was elucidated. Four groups of rats were used: control, ethanol (ulcer), omeprazole, and manuka honey. Stomachs were examined macroscopically for hemorrhagic lesions in the glandular mucosa, histopathological changes, and glycoprotein detection. The effects of oxidative stress were investigated using the following indicators: gastric mucosal nitric oxide (NO), reduced glutathione (GSH), lipid peroxide (MDA, measured as malondialdehyde) glutathione peroxidase (GPx), superoxide dismutase (SOD), and catalase. Plasma tumour necrosis factor-α, interleukin-1β, and IL-6 were also measured. Manuka honey significantly decreased the ulcer index, completely protected the mucosa from lesions, and preserved gastric mucosal glycoprotein. It significantly increased gastric mucosal levels of NO, GSH, GPx, and SOD. Manuka honey also decreased gastric mucosal MDA and plasma TNF-α, IL-1β, and IL-6 concentrations. In conclusion, manuka honey likely exerted its antiulcer, effect by keeping enzymatic (GPx and SOD) and nonenzymatic (GSH and NO) antioxidants as well as inflammatory cytokines (TNF-α, IL-1β, and IL-6) in a reduced form, inhibited lipid peroxidation (MDA), and preserved mucous glycoproteins levels.</abstract><cop>Cairo, Egypt</cop><pub>Hindawi Publishing Corporation</pub><pmid>26770649</pmid><doi>10.1155/2016/3643824</doi><tpages>10</tpages><orcidid>https://orcid.org/0000-0001-7512-8787</orcidid><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central Open Access; Wiley-Blackwell Open Access Titles; PubMed Central; Alma/SFX Local Collection |
| subjects | Animals Anti-Inflammatory Agents - pharmacology Anti-Inflammatory Agents - therapeutic use Anti-inflammatory drugs Antioxidants Antioxidants - pharmacology Antioxidants - therapeutic use Blood Glucose - metabolism Catalase - metabolism Cholesterol - blood Cytokines Disease Models, Animal Drinking Behavior - drug effects Drug dosages Enzymes Ethanol Feeding Behavior - drug effects Flavonoids Glutathione - metabolism Glutathione Peroxidase - metabolism Glycoproteins - metabolism Honey Interleukin-1beta - blood Interleukin-6 - blood Interleukins Lipid peroxidation Lipids Male Malondialdehyde - metabolism Medical research Nitric oxide Nitric Oxide - metabolism Omeprazole Rats Research centers Rodents Staining and Labeling Stomach Ulcer - drug therapy Stomach Ulcer - pathology Studies Superoxide Superoxide Dismutase - metabolism Toxicology Triglycerides - blood Tumor Necrosis Factor-alpha - blood Tumor necrosis factor-TNF Ulcers Weight Gain - drug effects |
| title | Antioxidant, Anti-inflammatory, and Antiulcer Potential of Manuka Honey against Gastric Ulcer in Rats |
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