CAJ | 학술논문

目的：探讨谷氨酰胺对大鼠缺血再灌注肠黏膜的作用及其可能机制。方法：成年雄性Wistar大鼠30只随机分为假手术组（ sham组）、缺血再灌注损伤组（ I/R组）和谷氨酰胺治疗组（ Gln组）。 Gln组给予谷氨酰胺1 g· kg-1· d-1连续灌胃7 d。 Sham 组和I/R组以同等剂量生理盐水灌胃7 d。 Sham 组仅分离肠系膜上动脉（ SMA）而不夹闭根部。 I/R组和Gln组均用无损伤血管夹夹闭SMA根部，30 min后放松血管夹形成再灌注损伤模型。各组大鼠均于制模后24 h采集静脉血和回肠标本。检测血清D-乳酸、内毒素、超氧化物歧化酶（ SOD ）和丙二醛（ MDA）水平，HE染色法观察肠组织病理损伤情况。结果：I/R组的D-乳酸、内毒素、MDA水平和Chiu's病理评分均高于sham组和Gln组（P＜0．05），血清SOD活力均低于sham组和Gln组（P＜0.05）。结论：谷氨酰胺对缺血再灌注损伤的肠黏膜屏障具有保护作用，其机制可能与抗氧化应激反应有关。
목적：탐토곡안선알대대서결혈재관주장점막적작용급기가능궤제。방법：성년웅성Wistar대서30지수궤분위가수술조（ sham조）、결혈재관주손상조（ I/R조）화곡안선알치료조（ Gln조）。 Gln조급여곡안선알1 g· kg-1· d-1련속관위7 d。 Sham 조화I/R조이동등제량생리염수관위7 d。 Sham 조부분리장계막상동맥（ SMA）이불협폐근부。 I/R조화Gln조균용무손상혈관협협폐SMA근부，30 min후방송혈관협형성재관주손상모형。각조대서균우제모후24 h채집정맥혈화회장표본。검측혈청D-유산、내독소、초양화물기화매（ SOD ）화병이철（ MDA）수평，HE염색법관찰장조직병리손상정황。결과：I/R조적D-유산、내독소、MDA수평화Chiu's병리평분균고우sham조화Gln조（P＜0．05），혈청SOD활력균저우sham조화Gln조（P＜0.05）。결론：곡안선알대결혈재관주손상적장점막병장구유보호작용，기궤제가능여항양화응격반응유관。
AIM:To determine the effects of glutamine ( Gln) pretreatment on intestinal ischemia-reperfusion (I/R) injury in the rats.METHODS: Thirty male Wistar rats were randomly divided into 3 groups (n=10): sham group, I/R group and Gln pretreatment group .The rats in Gln pretreatment group were pretreated with 1 g· kg -1 · d-1 Gln by orogastric route for 7 d, the rats in the other 2 groups were pretreated with normal saline .Intestinal I/R was induced by 30-min occlusion of the superior mesenteric artery followed by 24 h of reperfusion .After the operation , the plasma endo-toxin, serum D-lactic acid, superoxide dismutase ( SOD) and malondialdehyde ( MDA) levels were measured .The intesti-nal mucosal injury was observed with HE staining and evaluated using Chiu 's scoring.RESULTS: Serum D-lactic acid, endotoxin level , MDA level and Chiu's score in I/R group were significantly higher than those in sham group and Gln group (all P<0.05).Serum SOD activity was significantly lower than that in sham group and Gln group (P<0.05).CON-CLUSION:Glutamine has a protective effect on the intestines during ischemia-reperfusion injury .The mechanism may be related to oxidative stress response .