目的： 探讨大鼠肾缺血再灌注损伤（RIRI）模型对肠的影响以及莱菔硫烷的抗氧化保护作用。方法： Wistar 大鼠随机分为对照组、模型组、缺血用药组和灌注用药组，制备RIRI 模型，缺血用药组大鼠在夹闭左侧 肾动脉后立即给予莱菔硫烷，灌注用药组大鼠为去除血管夹待肾脏恢复血液灌注后立即给予莱菔硫烷。肾缺血再 灌注24 h 后，取血、肾和肠。H-E 染色光镜下观察大鼠肾、肠组织病理变化情况，应用生化自动分析仪检测血清 中氧化应激时的生化指标的变化，实时定量RT-PCR 检测大鼠肠组织超氧化物歧化酶（SOD）基因表达水平，免 疫印迹检测大鼠肠组织SOD蛋白水平的变化。结果：H-E 染色显示模型组、缺血用药组和灌注用药组小肠组织 的形态结构与对照组相比未见明显区别；模型组、缺血用药组、灌注用药组大鼠肠组织肌酐、尿素氮、丙二醛 含量、过氧化氢与对照组相比均明显升高，缺血用药组、灌注用药组又低于模型组，缺血用药组又低于灌注用 药组；模型组、缺血用药组、灌注用药组大鼠肠组织SOD活性与对照组相比均明显降低，缺血用药组和灌注用 药组SOD活性明显高于模型组，缺血用药组又高于灌注用药组；RIRI 组、缺血用药组、灌注用药组大鼠肠组织 SOD mRNA表达、SOD蛋白表达与对照组相比均明显升高，缺血用药组和灌注用药组明显高于模型组，但缺血 用药组和灌注用药组SOD mRNA表达、SOD蛋白表达无明显差别。结论：RIRI 可造成肠组织过氧化损伤，使肠 组织处于高度的氧化应激状态。RIRI 发生后，莱菔硫烷增强机体对ROS的清除作用，降低了肠组织的过氧化损 伤程度。缺血后即刻给予莱菔硫烷，与再灌注后给药相比，更能有效降低肠组织过氧化损伤程度。

Objective ： To investigate the influence of a rat model of renal ischemia-reperfusion injury （RIRI） on the intestine and the antioxidant protective effect of sulforaphane. Methods ：Wistar rats were randomly divided into the control group， model group， ischemia medication group， and perfusion medication group. The RIRI model was prepared， The rats in the ischemia medication group were given sulforaphane immediately after clipping the left renal artery， while in the perfusion medication group， sulforaphane was given instantaneously to the rats when the blood perfusion of their kidney was recovered after the vascular clamp was removed. Blood， kidney and intestine were collected 24 h after renal ischemia-reperfusion. The pathological changes of rat kidney and intestinal tissue were observed under the light microscope after H-E staining. The changes of biochemical indexes in serum during oxidative stress were detected by the biochemical automatic analyzer. The detection of expression level of superoxide dismutase （SOD） gene in rat intestinal tissue was carried out by real-time quantitative RT-PCR， and the changes of SOD protein level in rat intestinal tissue were detected by Western blotting. Results ： Under the light microscope after H-E staining， compared with the control group， there was no significant difference in the morphological structure of the small intestine in the model group， the ischemia medication group， and theperfusion medication group ； the contents of serum creatinine， blood urea nitrogen， malondialdehyde， and H2O2 in the model group， ischemia medication group， and perfusion medication group significantly higher than the control group. In addition， these in the — 335 — ischemia medication group and perfusion medication group were less than the model group， while in the ischemia medication group was lower than the perfusion medication group ； the SOD activity in the intestinal tissue of the rats in the model group， the ischemia medication group and the perfusion medicationgroup was obviously lower than that in the control group. Moreover， the SOD activity in ischemia medication group and perfusion medication group was significantly higher than that in model group， while that in ischemia medication group was higher than that in perfusion medication group. The expression of SOD mRNA and the expression of SOD protein in the model group， ischemia medication group and perfusion medication group were significantly higher than that in the control group. Furthermore， these in the ischemia medication group and perfusion medication group were higher than the model group， while there were no significant differences between the ischemia medication group and the perfusion medication group. Conclusions ： RIRI could cause peroxidative damage to intestinal tissue， making intestinal tissue in a state of high oxidative stress. Sulforaphane could enhance the scavenging effect on ROS and reduced the degree of peroxidative damage in intestinal tissue after the occurrence of RIRI. Additionally， immediate administration of sulforaphane after ischemia could reduce the degree of peroxidation injury of intestinal tissue more effectively than that after reperfusion.