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The intervention of tert-butylhydroquinone protects ethanol-induced gastric ulcer in type II diabetic rats: the role of Nrf2 pathway
Ethanol consumption increases the prevalence of gastric ulcer (GU) in rats with type II diabetes (T2D). Induction of GU by absolute ethanol (5 mL/kg or 3.94 g/kg) in the animal model resembles human ulcer characteristics. The aim was to investigate the role of the nuclear factor erythroid 2–related...
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| Published in: | Canadian journal of physiology and pharmacology 2021-05, Vol.99 (5), p.522-535 |
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| container_end_page | 535 |
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| container_title | Canadian journal of physiology and pharmacology |
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| creator | Rahman, Ziaur Dwivedi, Durgesh Kumar Jena, G.B |
| description | Ethanol consumption increases the prevalence of gastric ulcer (GU) in rats with type II diabetes (T2D). Induction of GU by absolute ethanol (5 mL/kg or 3.94 g/kg) in the animal model resembles human ulcer characteristics. The aim was to investigate the role of the nuclear factor erythroid 2–related factor 2 (Nrf2) pathway in the treatment of GU in diabetic condition. The rats were exposed to absolute ethanol 1 h before sacrifice and T2D was induced by combined exposure of high-fat diet and low dose streptozotocin. Pretreatment of tert-butylhydroquinone (tBHQ) (25 and 50 mg/kg), metformin (500 mg/kg), and omeprazole (20 mg/kg) were given once daily for last three consecutive weeks. In ethanol-exposed diabetic rats, pretreatment with tBHQ, omeprazole, and metformin reduced gastric mucosal lesion, ulcer index, histological alterations, malondialdehyde level, and apoptosis. Furthermore, the intervention of tBHQ, omeprazole, and metformin improved the integrity of the stomach mucosa, glutathione, gastric pH, collagen, and goblet cells. tBHQ treatment improved ethanol-induced alterations of Nrf2, catalase, heat shock protein 70 (HSP70), NF-κB, and endothelin-1 expressions in diabetic rats. In diabetic conditions, the incidence of GU is increased due to elevated levels of reactive oxygen species, inflammatory mediators, depleted levels of cellular antioxidants, and altered gastric parameters. The tBHQ intervention could be a rational strategy to protect these changes. |
| doi_str_mv | 10.1139/cjpp-2020-0173 |
| format | article |
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Induction of GU by absolute ethanol (5 mL/kg or 3.94 g/kg) in the animal model resembles human ulcer characteristics. The aim was to investigate the role of the nuclear factor erythroid 2–related factor 2 (Nrf2) pathway in the treatment of GU in diabetic condition. The rats were exposed to absolute ethanol 1 h before sacrifice and T2D was induced by combined exposure of high-fat diet and low dose streptozotocin. Pretreatment of tert-butylhydroquinone (tBHQ) (25 and 50 mg/kg), metformin (500 mg/kg), and omeprazole (20 mg/kg) were given once daily for last three consecutive weeks. In ethanol-exposed diabetic rats, pretreatment with tBHQ, omeprazole, and metformin reduced gastric mucosal lesion, ulcer index, histological alterations, malondialdehyde level, and apoptosis. Furthermore, the intervention of tBHQ, omeprazole, and metformin improved the integrity of the stomach mucosa, glutathione, gastric pH, collagen, and goblet cells. tBHQ treatment improved ethanol-induced alterations of Nrf2, catalase, heat shock protein 70 (HSP70), NF-κB, and endothelin-1 expressions in diabetic rats. In diabetic conditions, the incidence of GU is increased due to elevated levels of reactive oxygen species, inflammatory mediators, depleted levels of cellular antioxidants, and altered gastric parameters. The tBHQ intervention could be a rational strategy to protect these changes.</description><identifier>ISSN: 0008-4212</identifier><identifier>ISSN: 1205-7541</identifier><identifier>EISSN: 1205-7541</identifier><identifier>DOI: 10.1139/cjpp-2020-0173</identifier><identifier>PMID: 33095998</identifier><language>eng</language><publisher>1840 Woodward Drive, Suite 1, Ottawa, ON K2C 0P7: NRC Research Press</publisher><subject>Alcohol ; Alcohol, Denatured ; Animal models ; Animals ; Anti-Ulcer Agents - pharmacology ; Anti-Ulcer Agents - therapeutic use ; Antioxidants ; Antioxidants - pharmacology ; Antioxidants - therapeutic use ; Apoptosis ; Apoptosis - drug effects ; Care and treatment ; Catalase ; Causes of ; Collagen ; Diabetes ; Diabetes mellitus ; Diabetes Mellitus, Experimental - chemically induced ; Diabetes Mellitus, Experimental - complications ; Diabetes Mellitus, Experimental - drug therapy ; Diabetes Mellitus, Experimental - metabolism ; Diabetes Mellitus, Type 2 - chemically induced ; Diabetes Mellitus, Type 2 - complications ; Diabetes Mellitus, Type 2 - drug therapy ; Diabetes Mellitus, Type 2 - metabolism ; diabète sucré de type II ; Dosage ; Endothelin 1 ; Endothelins ; Ethanol ; Ethanol - adverse effects ; Ethanol - toxicity ; Gastric Mucosa - drug effects ; Gastric Mucosa - metabolism ; Gastric Mucosa - pathology ; gastric ulcer ; Glutathione ; Goblet cells ; Health aspects ; Heat shock proteins ; High fat diet ; Hsp70 protein ; Hydroquinone ; Hydroquinones - pharmacology ; Hydroquinones - therapeutic use ; Inflammation ; Low fat diet ; Male ; Malondialdehyde ; Metformin ; Metformin - pharmacology ; Metformin - therapeutic use ; Mucosa ; NF-E2-Related Factor 2 - metabolism ; NF-κB protein ; Nrf2 ; Nutrient deficiency ; Omeprazole ; Oxidative Stress - drug effects ; pH effects ; Physiological aspects ; Prevention ; Rats ; Rats, Wistar ; Reactive oxygen species ; Rodents ; Signal Transduction - drug effects ; Stomach ulcer ; Stomach Ulcer - chemically induced ; Stomach Ulcer - drug therapy ; Stomach Ulcer - metabolism ; Stomach Ulcer - pathology ; Stomach Ulcer - prevention & control ; t-Butylhydroquinone ; tert-butylhydroquinone ; Transcription factors ; Type 2 diabetes ; type II diabetes mellitus ; Ulcers ; ulcère gastrique</subject><ispartof>Canadian journal of physiology and pharmacology, 2021-05, Vol.99 (5), p.522-535</ispartof><rights>COPYRIGHT 2021 NRC Research Press</rights><rights>2021 Published by NRC Research Press</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c565t-7aecc61c38d4f5ffb4b8fe41a0aca741014f2b718f1d6ed04d1ecd508f4e047c3</citedby><cites>FETCH-LOGICAL-c565t-7aecc61c38d4f5ffb4b8fe41a0aca741014f2b718f1d6ed04d1ecd508f4e047c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27923,27924</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33095998$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Rahman, Ziaur</creatorcontrib><creatorcontrib>Dwivedi, Durgesh Kumar</creatorcontrib><creatorcontrib>Jena, G.B</creatorcontrib><title>The intervention of tert-butylhydroquinone protects ethanol-induced gastric ulcer in type II diabetic rats: the role of Nrf2 pathway</title><title>Canadian journal of physiology and pharmacology</title><addtitle>Can J Physiol Pharmacol</addtitle><description>Ethanol consumption increases the prevalence of gastric ulcer (GU) in rats with type II diabetes (T2D). Induction of GU by absolute ethanol (5 mL/kg or 3.94 g/kg) in the animal model resembles human ulcer characteristics. The aim was to investigate the role of the nuclear factor erythroid 2–related factor 2 (Nrf2) pathway in the treatment of GU in diabetic condition. The rats were exposed to absolute ethanol 1 h before sacrifice and T2D was induced by combined exposure of high-fat diet and low dose streptozotocin. Pretreatment of tert-butylhydroquinone (tBHQ) (25 and 50 mg/kg), metformin (500 mg/kg), and omeprazole (20 mg/kg) were given once daily for last three consecutive weeks. In ethanol-exposed diabetic rats, pretreatment with tBHQ, omeprazole, and metformin reduced gastric mucosal lesion, ulcer index, histological alterations, malondialdehyde level, and apoptosis. Furthermore, the intervention of tBHQ, omeprazole, and metformin improved the integrity of the stomach mucosa, glutathione, gastric pH, collagen, and goblet cells. tBHQ treatment improved ethanol-induced alterations of Nrf2, catalase, heat shock protein 70 (HSP70), NF-κB, and endothelin-1 expressions in diabetic rats. In diabetic conditions, the incidence of GU is increased due to elevated levels of reactive oxygen species, inflammatory mediators, depleted levels of cellular antioxidants, and altered gastric parameters. The tBHQ intervention could be a rational strategy to protect these changes.</description><subject>Alcohol</subject><subject>Alcohol, Denatured</subject><subject>Animal models</subject><subject>Animals</subject><subject>Anti-Ulcer Agents - pharmacology</subject><subject>Anti-Ulcer Agents - therapeutic use</subject><subject>Antioxidants</subject><subject>Antioxidants - pharmacology</subject><subject>Antioxidants - therapeutic use</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Care and treatment</subject><subject>Catalase</subject><subject>Causes of</subject><subject>Collagen</subject><subject>Diabetes</subject><subject>Diabetes mellitus</subject><subject>Diabetes Mellitus, Experimental - chemically induced</subject><subject>Diabetes Mellitus, Experimental - complications</subject><subject>Diabetes Mellitus, Experimental - drug therapy</subject><subject>Diabetes Mellitus, Experimental - metabolism</subject><subject>Diabetes Mellitus, Type 2 - chemically induced</subject><subject>Diabetes Mellitus, Type 2 - complications</subject><subject>Diabetes Mellitus, Type 2 - drug therapy</subject><subject>Diabetes Mellitus, Type 2 - metabolism</subject><subject>diabète sucré de type II</subject><subject>Dosage</subject><subject>Endothelin 1</subject><subject>Endothelins</subject><subject>Ethanol</subject><subject>Ethanol - adverse effects</subject><subject>Ethanol - toxicity</subject><subject>Gastric Mucosa - drug effects</subject><subject>Gastric Mucosa - metabolism</subject><subject>Gastric Mucosa - pathology</subject><subject>gastric ulcer</subject><subject>Glutathione</subject><subject>Goblet cells</subject><subject>Health aspects</subject><subject>Heat shock proteins</subject><subject>High fat diet</subject><subject>Hsp70 protein</subject><subject>Hydroquinone</subject><subject>Hydroquinones - pharmacology</subject><subject>Hydroquinones - therapeutic use</subject><subject>Inflammation</subject><subject>Low fat diet</subject><subject>Male</subject><subject>Malondialdehyde</subject><subject>Metformin</subject><subject>Metformin - pharmacology</subject><subject>Metformin - therapeutic use</subject><subject>Mucosa</subject><subject>NF-E2-Related Factor 2 - metabolism</subject><subject>NF-κB protein</subject><subject>Nrf2</subject><subject>Nutrient deficiency</subject><subject>Omeprazole</subject><subject>Oxidative Stress - drug effects</subject><subject>pH effects</subject><subject>Physiological aspects</subject><subject>Prevention</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Reactive oxygen species</subject><subject>Rodents</subject><subject>Signal Transduction - drug effects</subject><subject>Stomach ulcer</subject><subject>Stomach Ulcer - chemically induced</subject><subject>Stomach Ulcer - drug therapy</subject><subject>Stomach Ulcer - metabolism</subject><subject>Stomach Ulcer - pathology</subject><subject>Stomach Ulcer - prevention & control</subject><subject>t-Butylhydroquinone</subject><subject>tert-butylhydroquinone</subject><subject>Transcription factors</subject><subject>Type 2 diabetes</subject><subject>type II diabetes mellitus</subject><subject>Ulcers</subject><subject>ulcère gastrique</subject><issn>0008-4212</issn><issn>1205-7541</issn><issn>1205-7541</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><recordid>eNqVkk1v1DAQhiMEokvhyhFZcIFDiu3YSba3quJjpapIUM6WY493vcraqe0AufPDcdTlY9FKCPlgzfiZd8ajtyieEnxGSLV8rbbDUFJMcYlJU90rFoRiXjackfvFAmPclowSelI8inGbw7qt2ofFSVXhJV8u20Xx_WYDyLoE4Qu4ZL1D3qAcpbIb09RvJh387Widd4CG4BOoFBGkjXS-L63TowKN1jKmYBUaewUhq6E0DYBWK6St7CDllyBTPEcp9wq-h7nHdTAUDTJtvsrpcfHAyD7Ck_19Wnx---bm8n159eHd6vLiqlS85qlsJChVE1W1mhluTMe61gAjEkslG0YwYYZ2DWkN0TVozDQBpTluDQPMGlWdFi_vdIf5UxCT2NmooO-lAz9GQVneW8Xammb0xV_o1o_B5ekE5ZQ3Fa5p_Ztayx6EdcanINUsKi7qmjOOaTVT5RFqDQ6C7PNijc3pA_75EV4N9lb8CZ0dgfLRsLPqqOqrg4LMJPiW1nKMUaw-ffwP9vqQ3Q-igo8xgBFDsDsZJkGwmD0qZo-K2aNi9mgueLZf7djtQP_Cf5oyA-QOcEEFiCCD2vxL9AfFTu_r</recordid><startdate>20210501</startdate><enddate>20210501</enddate><creator>Rahman, Ziaur</creator><creator>Dwivedi, Durgesh Kumar</creator><creator>Jena, G.B</creator><general>NRC Research Press</general><general>Canadian Science Publishing NRC Research Press</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>ISN</scope><scope>ISR</scope><scope>7QP</scope><scope>7QR</scope><scope>7TK</scope><scope>8FD</scope><scope>FR3</scope><scope>K9.</scope><scope>NAPCQ</scope><scope>P64</scope><scope>7X8</scope></search><sort><creationdate>20210501</creationdate><title>The intervention of tert-butylhydroquinone protects ethanol-induced gastric ulcer in type II diabetic rats: the role of Nrf2 pathway</title><author>Rahman, Ziaur ; Dwivedi, Durgesh Kumar ; Jena, G.B</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c565t-7aecc61c38d4f5ffb4b8fe41a0aca741014f2b718f1d6ed04d1ecd508f4e047c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Alcohol</topic><topic>Alcohol, Denatured</topic><topic>Animal models</topic><topic>Animals</topic><topic>Anti-Ulcer Agents - pharmacology</topic><topic>Anti-Ulcer Agents - therapeutic use</topic><topic>Antioxidants</topic><topic>Antioxidants - pharmacology</topic><topic>Antioxidants - therapeutic use</topic><topic>Apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>Care and treatment</topic><topic>Catalase</topic><topic>Causes of</topic><topic>Collagen</topic><topic>Diabetes</topic><topic>Diabetes mellitus</topic><topic>Diabetes Mellitus, Experimental - chemically induced</topic><topic>Diabetes Mellitus, Experimental - complications</topic><topic>Diabetes Mellitus, Experimental - drug therapy</topic><topic>Diabetes Mellitus, Experimental - metabolism</topic><topic>Diabetes Mellitus, Type 2 - chemically induced</topic><topic>Diabetes Mellitus, Type 2 - complications</topic><topic>Diabetes Mellitus, Type 2 - drug therapy</topic><topic>Diabetes Mellitus, Type 2 - metabolism</topic><topic>diabète sucré de type II</topic><topic>Dosage</topic><topic>Endothelin 1</topic><topic>Endothelins</topic><topic>Ethanol</topic><topic>Ethanol - adverse effects</topic><topic>Ethanol - toxicity</topic><topic>Gastric Mucosa - drug effects</topic><topic>Gastric Mucosa - metabolism</topic><topic>Gastric Mucosa - pathology</topic><topic>gastric ulcer</topic><topic>Glutathione</topic><topic>Goblet cells</topic><topic>Health aspects</topic><topic>Heat shock proteins</topic><topic>High fat diet</topic><topic>Hsp70 protein</topic><topic>Hydroquinone</topic><topic>Hydroquinones - pharmacology</topic><topic>Hydroquinones - therapeutic use</topic><topic>Inflammation</topic><topic>Low fat diet</topic><topic>Male</topic><topic>Malondialdehyde</topic><topic>Metformin</topic><topic>Metformin - pharmacology</topic><topic>Metformin - therapeutic use</topic><topic>Mucosa</topic><topic>NF-E2-Related Factor 2 - metabolism</topic><topic>NF-κB protein</topic><topic>Nrf2</topic><topic>Nutrient deficiency</topic><topic>Omeprazole</topic><topic>Oxidative Stress - drug effects</topic><topic>pH effects</topic><topic>Physiological aspects</topic><topic>Prevention</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Reactive oxygen species</topic><topic>Rodents</topic><topic>Signal Transduction - drug effects</topic><topic>Stomach ulcer</topic><topic>Stomach Ulcer - chemically induced</topic><topic>Stomach Ulcer - drug therapy</topic><topic>Stomach Ulcer - metabolism</topic><topic>Stomach Ulcer - pathology</topic><topic>Stomach Ulcer - prevention & control</topic><topic>t-Butylhydroquinone</topic><topic>tert-butylhydroquinone</topic><topic>Transcription factors</topic><topic>Type 2 diabetes</topic><topic>type II diabetes mellitus</topic><topic>Ulcers</topic><topic>ulcère gastrique</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Rahman, Ziaur</creatorcontrib><creatorcontrib>Dwivedi, Durgesh Kumar</creatorcontrib><creatorcontrib>Jena, G.B</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: Canada</collection><collection>Gale In Context: Science</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Canadian journal of physiology and pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Rahman, Ziaur</au><au>Dwivedi, Durgesh Kumar</au><au>Jena, G.B</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The intervention of tert-butylhydroquinone protects ethanol-induced gastric ulcer in type II diabetic rats: the role of Nrf2 pathway</atitle><jtitle>Canadian journal of physiology and pharmacology</jtitle><addtitle>Can J Physiol Pharmacol</addtitle><date>2021-05-01</date><risdate>2021</risdate><volume>99</volume><issue>5</issue><spage>522</spage><epage>535</epage><pages>522-535</pages><issn>0008-4212</issn><issn>1205-7541</issn><eissn>1205-7541</eissn><abstract>Ethanol consumption increases the prevalence of gastric ulcer (GU) in rats with type II diabetes (T2D). Induction of GU by absolute ethanol (5 mL/kg or 3.94 g/kg) in the animal model resembles human ulcer characteristics. The aim was to investigate the role of the nuclear factor erythroid 2–related factor 2 (Nrf2) pathway in the treatment of GU in diabetic condition. The rats were exposed to absolute ethanol 1 h before sacrifice and T2D was induced by combined exposure of high-fat diet and low dose streptozotocin. Pretreatment of tert-butylhydroquinone (tBHQ) (25 and 50 mg/kg), metformin (500 mg/kg), and omeprazole (20 mg/kg) were given once daily for last three consecutive weeks. In ethanol-exposed diabetic rats, pretreatment with tBHQ, omeprazole, and metformin reduced gastric mucosal lesion, ulcer index, histological alterations, malondialdehyde level, and apoptosis. Furthermore, the intervention of tBHQ, omeprazole, and metformin improved the integrity of the stomach mucosa, glutathione, gastric pH, collagen, and goblet cells. tBHQ treatment improved ethanol-induced alterations of Nrf2, catalase, heat shock protein 70 (HSP70), NF-κB, and endothelin-1 expressions in diabetic rats. In diabetic conditions, the incidence of GU is increased due to elevated levels of reactive oxygen species, inflammatory mediators, depleted levels of cellular antioxidants, and altered gastric parameters. The tBHQ intervention could be a rational strategy to protect these changes.</abstract><cop>1840 Woodward Drive, Suite 1, Ottawa, ON K2C 0P7</cop><pub>NRC Research Press</pub><pmid>33095998</pmid><doi>10.1139/cjpp-2020-0173</doi><tpages>14</tpages></addata></record> |
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| ispartof | Canadian journal of physiology and pharmacology, 2021-05, Vol.99 (5), p.522-535 |
| issn | 0008-4212 1205-7541 1205-7541 |
| language | eng |
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| source | EBSCOhost SPORTDiscus - Ebooks |
| subjects | Alcohol Alcohol, Denatured Animal models Animals Anti-Ulcer Agents - pharmacology Anti-Ulcer Agents - therapeutic use Antioxidants Antioxidants - pharmacology Antioxidants - therapeutic use Apoptosis Apoptosis - drug effects Care and treatment Catalase Causes of Collagen Diabetes Diabetes mellitus Diabetes Mellitus, Experimental - chemically induced Diabetes Mellitus, Experimental - complications Diabetes Mellitus, Experimental - drug therapy Diabetes Mellitus, Experimental - metabolism Diabetes Mellitus, Type 2 - chemically induced Diabetes Mellitus, Type 2 - complications Diabetes Mellitus, Type 2 - drug therapy Diabetes Mellitus, Type 2 - metabolism diabète sucré de type II Dosage Endothelin 1 Endothelins Ethanol Ethanol - adverse effects Ethanol - toxicity Gastric Mucosa - drug effects Gastric Mucosa - metabolism Gastric Mucosa - pathology gastric ulcer Glutathione Goblet cells Health aspects Heat shock proteins High fat diet Hsp70 protein Hydroquinone Hydroquinones - pharmacology Hydroquinones - therapeutic use Inflammation Low fat diet Male Malondialdehyde Metformin Metformin - pharmacology Metformin - therapeutic use Mucosa NF-E2-Related Factor 2 - metabolism NF-κB protein Nrf2 Nutrient deficiency Omeprazole Oxidative Stress - drug effects pH effects Physiological aspects Prevention Rats Rats, Wistar Reactive oxygen species Rodents Signal Transduction - drug effects Stomach ulcer Stomach Ulcer - chemically induced Stomach Ulcer - drug therapy Stomach Ulcer - metabolism Stomach Ulcer - pathology Stomach Ulcer - prevention & control t-Butylhydroquinone tert-butylhydroquinone Transcription factors Type 2 diabetes type II diabetes mellitus Ulcers ulcère gastrique |
| title | The intervention of tert-butylhydroquinone protects ethanol-induced gastric ulcer in type II diabetic rats: the role of Nrf2 pathway |
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