The effect of heme oxygenase-1 induction by glutamine on TNBS-induced colitis -: The effect of glutamine on TNBS colitis
The effect of heme oxygenase-1 induction by glutamine on TNBS-induced colitis -: The effect of glutamine on TNBS colitis
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DOI：
10.1007/s00384-006-0238-y
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发表时间：
2007-06-01
影响因子：
2.8
通讯作者：
Toker, Gulcin Aykac
中科院分区：
文献类型：
--
作者：
Giris, Murat;Erbil, Yesim;Toker, Gulcin Aykac
背景炎症性肠病是一种病因不明的多因素结肠和直肠炎性疾病。在本研究中，我们的目的是探讨血红素氧合酶-1（HO-1）诱导谷氨酰胺是否可以保护结肠炎引起的氧化，炎症和凋亡损伤。I组仅给予TNBS结肠炎，2组给予TNBS诱导的结肠炎，并在给予TNBS溶液前3天和给予TNBS溶液后15天灌胃谷氨酰胺1g/kg/天，3组仅给予谷氨酰胺1g/kg/天灌胃18天后处死，第4组仅用等渗盐水1cm（3）/只灌胃18天后处死。检测各组大鼠结肠组织丙二醛（MDA）含量、谷胱甘肽（GSH）含量、caspase-3活性和HO-1表达。结果与对照组相比，TNBS诱导的结肠炎大鼠结肠组织中MDA含量、caspase-3活性和HO-1表达均显著升高。谷氨酰胺处理与HO-1表达和GSH水平增加以及MDA水平和caspase-3活性降低相关。组织学检查显示，谷氨酰胺治疗组的肠粘膜结构得以保留。除此之外，谷氨酰胺治疗显着增加HO-1的表达和减少NFkB的表达，通过免疫组化相比，TNBS诱导的结肠炎group.Conclusion谷氨酰胺减少TNBS诱导的结肠炎的结肠损伤。与谷氨酰胺相关的保护机制是由于抗氧化、抗凋亡、抗炎和HO-1诱导作用。
Background Inflammatory bowel disease is a multifactorial inflammatory disease of the colon and rectum with an unknown etiology. In the present study, we aimed to investigate whether heme oxygenase-1 (HO-1) induction by glutamine could protect colitis-induced damage from oxidative, inflammatory, and apoptotic damage.Method The rats were divided into four groups. Group I had TNBS colitis alone, group 2 had TNBS-induced colitis and glutamine 1 g/kg/day intragastric gavage for 3 days before TNBS solution administration and 15 days following TNBS solution administration, group 3 had glutamine alone 1 g/kg/day intragastric gavage for 18 days before being killed, and group 4 had isotonic saline solution alone 1 cm(3)/rat intragastric gavage for 18 days before being killed. Colonic malondialdehyde (MDA) levels, glutathione (GSH) levels, caspase-3 activities, and HO-1 expressions of the killed rats were measured. Nuclear factor kappa B (NFKB) and HO-1 expression were evaluated by immunohistochemical examination of the colonic tissue.Result TNBS-induced colitis significantly increased the colonic MDA levels, caspase-3 activities, and HO-1 expression in comparison to the control group. Glutamine treatment was associated with increased HO-1 expression and GSH levels and decreased MDA levels and caspase-3 activity. Histopathological examination revealed that the intestinal mucosal structure was preserved in the glutamine-treated group. In addition to this, treatment with glutamine significantly increased HO-1 expression and decreased NFkB expression by immunohistochemistry when compared to the TNBS-induced colitis group.Conclusion Glutamine reduced colonic damage in TNBS-induced colitis. The mechanism of the protection associated with glutamine was due to antioxidant, antiapoptotic, anti-inflammatory, and HO-1 induction effects.