Giriş Murat, Erbil Yeşim, Doğru-Abbasoğlu Semra, Yanik Burcu Tulumoğlu, Aliş Halil, Olgaç Vakur, Toker Gülçin Aykaç
Department of Biochemistry, Istanbul Medical Faculty, Istanbul University, Capa, Istanbul, Turkey.
Int J Colorectal Dis. 2007 Jun;22(6):591-9. doi: 10.1007/s00384-006-0238-y. Epub 2006 Nov 24.
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.
The rats were divided into four groups. Group 1 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 cm3/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 (NF-kappaB) and HO-1 expression were evaluated by immunohistochemical examination of the colonic tissue.
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 NF-kappaB expression by immunohistochemistry when compared to the TNBS-induced colitis group.
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.
炎症性肠病是一种结肠和直肠的多因素炎症性疾病，病因不明。在本研究中，我们旨在探讨谷氨酰胺诱导的血红素加氧酶-1（HO-1）是否能保护结肠炎引起的氧化、炎症和凋亡损伤。
将大鼠分为四组。第1组仅患有三硝基苯磺酸（TNBS）诱导的结肠炎，第2组在给予TNBS溶液前3天及给予TNBS溶液后15天，每天经胃内灌胃1 g/kg谷氨酰胺，患有TNBS诱导的结肠炎，第3组在处死前18天每天经胃内灌胃1 g/kg谷氨酰胺，第4组在处死前18天每天经胃内给每只大鼠灌胃1 cm³等渗盐溶液。测定处死大鼠的结肠丙二醛（MDA）水平、谷胱甘肽（GSH）水平、半胱天冬酶-3（caspase-3）活性和HO-1表达。通过结肠组织的免疫组织化学检查评估核因子κB（NF-κB）和HO-1表达。
与对照组相比，TNBS诱导的结肠炎显著增加了结肠MDA水平、caspase-3活性和HO-1表达。谷氨酰胺治疗与HO-1表达增加、GSH水平升高以及MDA水平和caspase-3活性降低有关。组织病理学检查显示，谷氨酰胺治疗组的肠黏膜结构得以保留。除此之外，与TNBS诱导的结肠炎组相比，谷氨酰胺治疗通过免疫组织化学显著增加了HO-1表达并降低了NF-κB表达。
谷氨酰胺减轻了TNBS诱导的结肠炎中的结肠损伤。谷氨酰胺相关保护作用的机制归因于抗氧化、抗凋亡、抗炎和诱导HO-1的作用。
