EFFECTS OF SOFALCONE ON NECROTIZING AGENTS-INDUCED GASTRIC LESIONS AND ON ENDOGENOUS PROSTAGLANDINS IN RATS STOMACHS
Attempts were made to investigate the effect of 2'-carboxymethoxy 4, 4'-bis (3-methyl-2-butenyloxy) chalcone (sofalcone) on necrotizing agents-induced gastric lesions and on prostaglandin E2 (PGE2)-like activity of the gastric tissue in rats. 1. Sofalcone, 100 mg/kg i.p. and 300 mg/kg p.o....
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| Veröffentlicht in: | Journal of Pharmacobio-Dynamics 1984, Vol.7(11), pp.791-797 |
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| container_title | Journal of Pharmacobio-Dynamics |
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| creator | SAZIKI, RYUICHI ARAI, IWAO ISOBE, YOSHIHIKO HIROSE, HARUKO AIHARA, HIRONAKA |
| description | Attempts were made to investigate the effect of 2'-carboxymethoxy 4, 4'-bis (3-methyl-2-butenyloxy) chalcone (sofalcone) on necrotizing agents-induced gastric lesions and on prostaglandin E2 (PGE2)-like activity of the gastric tissue in rats. 1. Sofalcone, 100 mg/kg i.p. and 300 mg/kg p.o., markedly suppressed 0.6 N HCl-or 100% Et0H-induced gastric lesions. Sofalcone, 100 mg/kg i.p., also significantly suppressed 0.2N NaOH-induced gastric lesions. 2. Sofalcone suppressed 0.6 N HCl-induced gastric lesions with both oral and intraperitoneal routes, and the effect was particularly marked at 60 min. A dose of 100 mg/kg i.p. showed suppression lasting for up to 300 min. 3. 0.6N HCl-induced gastric lesions were significantly aggravated by indomechacin treatment (10 mg/kg s.c.). Oral sofalcone (300 mg/kg) significantly suppressed the aggravation of gastric lesions by indomethacin given before and after sofalcone, but the i.p. (100 mg/kg) did not show significant suppression in the case of pretreatment with indomethacin. 4. PGs-like activity in the gastric tissue was increased in both of the fundus and the antrum by the administration of sofalcone without any dose-dependency. The increase was continuous and lasted for 6 h in the fundus of the stomach. |
| doi_str_mv | 10.1248/bpb1978.7.791 |
| format | Article |
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Sofalcone, 100 mg/kg i.p. and 300 mg/kg p.o., markedly suppressed 0.6 N HCl-or 100% Et0H-induced gastric lesions. Sofalcone, 100 mg/kg i.p., also significantly suppressed 0.2N NaOH-induced gastric lesions. 2. Sofalcone suppressed 0.6 N HCl-induced gastric lesions with both oral and intraperitoneal routes, and the effect was particularly marked at 60 min. A dose of 100 mg/kg i.p. showed suppression lasting for up to 300 min. 3. 0.6N HCl-induced gastric lesions were significantly aggravated by indomechacin treatment (10 mg/kg s.c.). Oral sofalcone (300 mg/kg) significantly suppressed the aggravation of gastric lesions by indomethacin given before and after sofalcone, but the i.p. (100 mg/kg) did not show significant suppression in the case of pretreatment with indomethacin. 4. PGs-like activity in the gastric tissue was increased in both of the fundus and the antrum by the administration of sofalcone without any dose-dependency. The increase was continuous and lasted for 6 h in the fundus of the stomach.</description><identifier>ISSN: 0386-846X</identifier><identifier>EISSN: 1881-1353</identifier><identifier>DOI: 10.1248/bpb1978.7.791</identifier><identifier>PMID: 6597872</identifier><identifier>CODEN: JOPHDQ</identifier><language>eng</language><publisher>Tokyo: The Pharmaceutical Society of Japan</publisher><subject>Animals ; Anti-Ulcer Agents - pharmacology ; Anti-Ulcer Agents - therapeutic use ; Biological and medical sciences ; Chalcone - analogs & derivatives ; Chalcone - pharmacology ; Chalcone - therapeutic use ; Chalcones ; cytoprotection ; Digestive system ; Dinoprostone ; Gastric Mucosa - metabolism ; Indomethacin ; Male ; Medical sciences ; Necrosis ; Pharmacology. Drug treatments ; Propiophenones - pharmacology ; Prostaglandins - metabolism ; Prostaglandins E - metabolism ; Rats ; Rats, Inbred Strains ; Stomach Ulcer - chemically induced ; Stomach Ulcer - pathology ; Stomach Ulcer - prevention & control ; Time Factors</subject><ispartof>Journal of Pharmacobio-Dynamics, 1984, Vol.7(11), pp.791-797</ispartof><rights>The Pharmaceutical Society of Japan</rights><rights>1985 INIST-CNRS</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c573t-6eda9755c96ebf67fd4eaf79779a71dfdce70a05a919356082600464aa3cf3f63</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,1877,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=9244741$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/6597872$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>SAZIKI, RYUICHI</creatorcontrib><creatorcontrib>ARAI, IWAO</creatorcontrib><creatorcontrib>ISOBE, YOSHIHIKO</creatorcontrib><creatorcontrib>HIROSE, HARUKO</creatorcontrib><creatorcontrib>AIHARA, HIRONAKA</creatorcontrib><title>EFFECTS OF SOFALCONE ON NECROTIZING AGENTS-INDUCED GASTRIC LESIONS AND ON ENDOGENOUS PROSTAGLANDINS IN RATS STOMACHS</title><title>Journal of Pharmacobio-Dynamics</title><addtitle>Journal of Pharmacobio-Dynamics</addtitle><description>Attempts were made to investigate the effect of 2'-carboxymethoxy 4, 4'-bis (3-methyl-2-butenyloxy) chalcone (sofalcone) on necrotizing agents-induced gastric lesions and on prostaglandin E2 (PGE2)-like activity of the gastric tissue in rats. 1. Sofalcone, 100 mg/kg i.p. and 300 mg/kg p.o., markedly suppressed 0.6 N HCl-or 100% Et0H-induced gastric lesions. Sofalcone, 100 mg/kg i.p., also significantly suppressed 0.2N NaOH-induced gastric lesions. 2. Sofalcone suppressed 0.6 N HCl-induced gastric lesions with both oral and intraperitoneal routes, and the effect was particularly marked at 60 min. A dose of 100 mg/kg i.p. showed suppression lasting for up to 300 min. 3. 0.6N HCl-induced gastric lesions were significantly aggravated by indomechacin treatment (10 mg/kg s.c.). Oral sofalcone (300 mg/kg) significantly suppressed the aggravation of gastric lesions by indomethacin given before and after sofalcone, but the i.p. (100 mg/kg) did not show significant suppression in the case of pretreatment with indomethacin. 4. PGs-like activity in the gastric tissue was increased in both of the fundus and the antrum by the administration of sofalcone without any dose-dependency. The increase was continuous and lasted for 6 h in the fundus of the stomach.</description><subject>Animals</subject><subject>Anti-Ulcer Agents - pharmacology</subject><subject>Anti-Ulcer Agents - therapeutic use</subject><subject>Biological and medical sciences</subject><subject>Chalcone - analogs & derivatives</subject><subject>Chalcone - pharmacology</subject><subject>Chalcone - therapeutic use</subject><subject>Chalcones</subject><subject>cytoprotection</subject><subject>Digestive system</subject><subject>Dinoprostone</subject><subject>Gastric Mucosa - metabolism</subject><subject>Indomethacin</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Necrosis</subject><subject>Pharmacology. Drug treatments</subject><subject>Propiophenones - pharmacology</subject><subject>Prostaglandins - metabolism</subject><subject>Prostaglandins E - metabolism</subject><subject>Rats</subject><subject>Rats, Inbred Strains</subject><subject>Stomach Ulcer - chemically induced</subject><subject>Stomach Ulcer - pathology</subject><subject>Stomach Ulcer - prevention & control</subject><subject>Time Factors</subject><issn>0386-846X</issn><issn>1881-1353</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1984</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpNkD1PwzAQhi0EgvIxMiJ5YE2J68SOx8h1QqRgozqVEEvkOjYUFaiSMvDvcdWoYrkbnufudC8AtyieolmSPay2K8RoNqVTytAJmKAsQxHCKT4FkxhnJMoS8nIBLofhI44TlqXoHJyTNIzQ2QTsRFEI3mioCqhVkddcSQGVhFLwhWqq10qWMC-FbHRUyfmSizksc90sKg5roSslNczlfD8h5FwFUS01fF4o3eRlHUgVhErCRR5u6EY95fxRX4MzbzaDuxn7FVgWouGPUa3Kiud1ZFOKdxFxnWE0TS0jbuUJ9V3ijKeMUmYo6nxnHY1NnBqGGE5JnM1I-JAkxmDrsSf4CkSHvbb_Hobe-Xbbrz9N_9uiuN2H147htbQN4QX_7uBvf1afrjvaY1qB34_cDNZsfG--7Ho4amyWJDTZr-EH7WPYmTd35Kbfre3G_TuK0FgYOlL7bvrWfeE_ZCuF9g</recordid><startdate>19840101</startdate><enddate>19840101</enddate><creator>SAZIKI, RYUICHI</creator><creator>ARAI, IWAO</creator><creator>ISOBE, YOSHIHIKO</creator><creator>HIROSE, HARUKO</creator><creator>AIHARA, HIRONAKA</creator><general>The Pharmaceutical Society of Japan</general><general>Pharmaceutical Society of Japan</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope></search><sort><creationdate>19840101</creationdate><title>EFFECTS OF SOFALCONE ON NECROTIZING AGENTS-INDUCED GASTRIC LESIONS AND ON ENDOGENOUS PROSTAGLANDINS IN RATS STOMACHS</title><author>SAZIKI, RYUICHI ; ARAI, IWAO ; ISOBE, YOSHIHIKO ; HIROSE, HARUKO ; AIHARA, HIRONAKA</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c573t-6eda9755c96ebf67fd4eaf79779a71dfdce70a05a919356082600464aa3cf3f63</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1984</creationdate><topic>Animals</topic><topic>Anti-Ulcer Agents - pharmacology</topic><topic>Anti-Ulcer Agents - therapeutic use</topic><topic>Biological and medical sciences</topic><topic>Chalcone - analogs & derivatives</topic><topic>Chalcone - pharmacology</topic><topic>Chalcone - therapeutic use</topic><topic>Chalcones</topic><topic>cytoprotection</topic><topic>Digestive system</topic><topic>Dinoprostone</topic><topic>Gastric Mucosa - metabolism</topic><topic>Indomethacin</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Necrosis</topic><topic>Pharmacology. Drug treatments</topic><topic>Propiophenones - pharmacology</topic><topic>Prostaglandins - metabolism</topic><topic>Prostaglandins E - metabolism</topic><topic>Rats</topic><topic>Rats, Inbred Strains</topic><topic>Stomach Ulcer - chemically induced</topic><topic>Stomach Ulcer - pathology</topic><topic>Stomach Ulcer - prevention & control</topic><topic>Time Factors</topic><toplevel>online_resources</toplevel><creatorcontrib>SAZIKI, RYUICHI</creatorcontrib><creatorcontrib>ARAI, IWAO</creatorcontrib><creatorcontrib>ISOBE, YOSHIHIKO</creatorcontrib><creatorcontrib>HIROSE, HARUKO</creatorcontrib><creatorcontrib>AIHARA, HIRONAKA</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><jtitle>Journal of Pharmacobio-Dynamics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>SAZIKI, RYUICHI</au><au>ARAI, IWAO</au><au>ISOBE, YOSHIHIKO</au><au>HIROSE, HARUKO</au><au>AIHARA, HIRONAKA</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>EFFECTS OF SOFALCONE ON NECROTIZING AGENTS-INDUCED GASTRIC LESIONS AND ON ENDOGENOUS PROSTAGLANDINS IN RATS STOMACHS</atitle><jtitle>Journal of Pharmacobio-Dynamics</jtitle><addtitle>Journal of Pharmacobio-Dynamics</addtitle><date>1984-01-01</date><risdate>1984</risdate><volume>7</volume><issue>11</issue><spage>791</spage><epage>797</epage><pages>791-797</pages><issn>0386-846X</issn><eissn>1881-1353</eissn><coden>JOPHDQ</coden><abstract>Attempts were made to investigate the effect of 2'-carboxymethoxy 4, 4'-bis (3-methyl-2-butenyloxy) chalcone (sofalcone) on necrotizing agents-induced gastric lesions and on prostaglandin E2 (PGE2)-like activity of the gastric tissue in rats. 1. Sofalcone, 100 mg/kg i.p. and 300 mg/kg p.o., markedly suppressed 0.6 N HCl-or 100% Et0H-induced gastric lesions. Sofalcone, 100 mg/kg i.p., also significantly suppressed 0.2N NaOH-induced gastric lesions. 2. Sofalcone suppressed 0.6 N HCl-induced gastric lesions with both oral and intraperitoneal routes, and the effect was particularly marked at 60 min. A dose of 100 mg/kg i.p. showed suppression lasting for up to 300 min. 3. 0.6N HCl-induced gastric lesions were significantly aggravated by indomechacin treatment (10 mg/kg s.c.). Oral sofalcone (300 mg/kg) significantly suppressed the aggravation of gastric lesions by indomethacin given before and after sofalcone, but the i.p. (100 mg/kg) did not show significant suppression in the case of pretreatment with indomethacin. 4. PGs-like activity in the gastric tissue was increased in both of the fundus and the antrum by the administration of sofalcone without any dose-dependency. The increase was continuous and lasted for 6 h in the fundus of the stomach.</abstract><cop>Tokyo</cop><pub>The Pharmaceutical Society of Japan</pub><pmid>6597872</pmid><doi>10.1248/bpb1978.7.791</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Anti-Ulcer Agents - pharmacology Anti-Ulcer Agents - therapeutic use Biological and medical sciences Chalcone - analogs & derivatives Chalcone - pharmacology Chalcone - therapeutic use Chalcones cytoprotection Digestive system Dinoprostone Gastric Mucosa - metabolism Indomethacin Male Medical sciences Necrosis Pharmacology. Drug treatments Propiophenones - pharmacology Prostaglandins - metabolism Prostaglandins E - metabolism Rats Rats, Inbred Strains Stomach Ulcer - chemically induced Stomach Ulcer - pathology Stomach Ulcer - prevention & control Time Factors |
| title | EFFECTS OF SOFALCONE ON NECROTIZING AGENTS-INDUCED GASTRIC LESIONS AND ON ENDOGENOUS PROSTAGLANDINS IN RATS STOMACHS |
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