The effect of heme oxygenase-1 induction by octreotide on radiation enteritis
The effect of heme oxygenase-1 induction by octreotide on radiation enteritis
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DOI：
10.1016/j.peptides.2005.11.012
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发表时间：
2006-06-01
期刊：
影响因子：
3
通讯作者：
Toker, Gulcin
中科院分区：
文献类型：
--
作者：
Abbasoglu, Semra Dogru;Erbil, Yesim;Toker, Gulcin
放射性肠炎是对腹部放射的反应，可引起胃肠道粘膜上皮的粘膜损伤。小肠是腹部对辐射最敏感的器官之一。本研究旨在观察奥曲肽（OCT）对放射性肠炎模型大鼠血红素氧合酶-1（HO-1）表达的影响。大鼠在照射前接受50 mg/kg/天OCT 4天，并在照射后继续接受3天。小肠髓过氧化物酶（MPO）活性、丙二醛（MDA）水平是氧化损伤的指标，而caspase-3活性则反映了小肠细胞凋亡的程度。在组织学检查时，分析末端回肠组织的形态学变化。与假手术对照组相比，照射组大鼠肠组织MPO、caspase-3活性、MDA含量及HO-1表达均显著升高。OCT治疗后HO-1表达和caspase-3活性增加，MPO活性和MDA水平降低。组织学检查显示，OCT治疗组的肠粘膜结构得以保留。OCT似乎对辐射引起的肠道损伤具有保护作用。这种保护作用部分是由炎症反应的修饰和HO-1表达的诱导介导的。(c)2005年爱思唯尔公司All rights reserved.
Radiation enteritis occurs as a response to abdominal radiation, which can cause mucosal damage in the gastrointestinal mucosal epithelium. The small intestine is one of the most radiosensitive organs in the abdomen. The present study was undertaken to investigate the effect of octreotide (OCT) administration on heme oxygenase-1 (HO-1) expression of the radiation enteritis model. Rats received 50 mg/kg/day OCT for 4 days before irradiation and continued for 3 days after irradiation. Intestinal myeloperoxidase (MPO) activities, malondialdehyde (MDA) levels are indicators of oxidative damage while caspase-3 activities reveal apoptosis degree of the small intestine. At histological examination, the terminal ileum tissue was analyzed for morphological changes. Irradiation significantly increased the intestinal MPO and caspase-3 activities, MDA levels and HO-1 expression in comparison to sham control group. OCT treatment was associated with increased HO-1 expression and caspase-3 activity, decreased MPO activity and MDA levels. Histological examination revealed that the intestinal mucosal structure was preserved in the OCT treated group. OCT appears to have protective effects against radiation-induced intestinal damage. This protective effect is, in part, mediated by modification of the inflammatory response and the induction of HO-1 expression. (c) 2005 Elsevier Inc. All rights reserved.