Effects of glucagon-like peptide-2 on TNF-alpha/actinomycin D-induced intestinal epithelial injury: a scanning electron microscopic and immunohistochemical study

P. A. Pirincci, P. Turan, S. Arbak, Ş. Bolkent
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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.
胰高血糖素样肽-2对tnf - α /放线菌素d诱导的肠上皮损伤的影响:扫描电镜和免疫组织化学研究
胰高血糖素样肽-2 (Glucagon-like peptide-2, GLP-2)是一种具有肠营养活性的肽激素,由肠道内分泌细胞释放。本研究旨在通过扫描电镜观察GLP-2在肿瘤坏死因子-α (TNF-α)/放线菌素D (Act D)诱导的肠上皮损伤中的作用,并探讨GLP-2的作用机制是否与胃肠激素如胆囊收缩素、生长抑素等介导有关。每只小鼠腹腔注射15µg/kg TNF-α和800µg/kg Act D诱导肠上皮损伤。在TNF-α和Act d给药前,连续10天每12小时皮下注射200µg/kg GLP-2类似物,扫描电镜检查显示TNF-α/Act d给药小鼠小肠严重上皮损伤。TNF-α/Act D可显著增加肠黏膜生长抑素免疫反应性内分泌细胞的数量,但不影响胆囊收缩素免疫反应性内分泌细胞的数量。另一方面,GLP-2类似物预处理通过显著减少生长抑素免疫反应性内分泌细胞的数量和退行性改变以及显著增加胆囊收缩素免疫反应性内分泌细胞的数量来预防TNF-α/Act d诱导的肠上皮损伤。因此,本研究提示GLP-2对TNF-α/Act d诱导的肠上皮损伤具有保护作用。GLP-2的保护作用可能与生长抑素和胆囊收缩素有关。
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