Effects of glucagon-like peptide-2 on TNF-alpha/actinomycin D-induced intestinal epithelial injury: a scanning electron microscopic and immunohistochemical study
{"title":"Effects of glucagon-like peptide-2 on TNF-alpha/actinomycin D-induced intestinal epithelial injury: a scanning electron microscopic and immunohistochemical study","authors":"P. A. Pirincci, P. Turan, S. Arbak, Ş. Bolkent","doi":"10.18478/IUFSJB.91609","DOIUrl":null,"url":null,"abstract":"Glucagon-like peptide-2 (GLP-2) is a peptide hormone with intestinotrophic activity, which is released from the intestinal endocrine cells. The aim of this study was to investigate the effects observed by scanning electron microscope of GLP-2 in intestinal epithelial injury induced by tumor necrosis factor-alpha (TNF-α)/actinomycin D (Act D). In addition, it aimed to elucidate whether the action mechanism of GLP-2 might be mediated by gastrointestinal hormones such as cholecystokinin and somatostatin . The intestinal epithelial injury was induced by intraperitoneal administration of 15 µg/kg TNF-α and 800 µg/kg Act D per mouse. Animals were injected subcutaneously 200 µg/kg GLP-2 analogue every 12 hr for 10 consecutive days prior to the administration of TNF-α and Act D. Scanning electron microscopic examination revealed severe epithelial damage in the small intestine of TNF-α/Act D-administered mice. The administration of TNF-α/Act D was significantly increased the number of somatostatin -immunoreactive endocrine cells, but did not affect the number of cholecystokinin -immunoreactive endocrine cells in the intestinal mucosa . On the other hand, GLP-2 analogue pretreatment prevented TNF-α/Act D-induced intestinal epithelial injury by causing a marked decrease in the degenerative changes and the number of somatostatin -immunoreactive endocrine cells, and a significant increase in the number of cholecystokinin -immunoreactive endocrine cells. As a result, the present study indicates that GLP-2 has a protective effect against TNF-α/Act D-induced intestinal epithelial injury. Morever protective effect of GLP-2 might be related to somatostatin and cholecystokinin.","PeriodicalId":14521,"journal":{"name":"IUFS Journal of Biology","volume":"80 1","pages":"27-38"},"PeriodicalIF":0.0000,"publicationDate":"2011-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"IUFS Journal of Biology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.18478/IUFSJB.91609","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
Glucagon-like peptide-2 (GLP-2) is a peptide hormone with intestinotrophic activity, which is released from the intestinal endocrine cells. The aim of this study was to investigate the effects observed by scanning electron microscope of GLP-2 in intestinal epithelial injury induced by tumor necrosis factor-alpha (TNF-α)/actinomycin D (Act D). In addition, it aimed to elucidate whether the action mechanism of GLP-2 might be mediated by gastrointestinal hormones such as cholecystokinin and somatostatin . The intestinal epithelial injury was induced by intraperitoneal administration of 15 µg/kg TNF-α and 800 µg/kg Act D per mouse. Animals were injected subcutaneously 200 µg/kg GLP-2 analogue every 12 hr for 10 consecutive days prior to the administration of TNF-α and Act D. Scanning electron microscopic examination revealed severe epithelial damage in the small intestine of TNF-α/Act D-administered mice. The administration of TNF-α/Act D was significantly increased the number of somatostatin -immunoreactive endocrine cells, but did not affect the number of cholecystokinin -immunoreactive endocrine cells in the intestinal mucosa . On the other hand, GLP-2 analogue pretreatment prevented TNF-α/Act D-induced intestinal epithelial injury by causing a marked decrease in the degenerative changes and the number of somatostatin -immunoreactive endocrine cells, and a significant increase in the number of cholecystokinin -immunoreactive endocrine cells. As a result, the present study indicates that GLP-2 has a protective effect against TNF-α/Act D-induced intestinal epithelial injury. Morever protective effect of GLP-2 might be related to somatostatin and cholecystokinin.