乳果糖预处理减轻大鼠肠缺血再灌注损伤的机制研究

 目的： 探讨乳果糖预处理对大鼠肠缺血再灌注损伤的影响及其作用机制。方法： 随机将30只SD大鼠分成假手术组、缺血再灌注组和乳果糖预处理组。乳果糖预处理组在手术前7 d每天给予乳果糖灌胃，假手术组和缺血再灌注组在手术前7 d每天给予等量生理盐水灌胃。手术分离肠系膜上动脉，通过夹闭30 min、再灌注60 min诱导缺血再灌注损伤。收集血清检测白细胞介素6（IL-6）、肿瘤坏死因子α(TNF-α)和IL-1β水平。HE染色用来评估组织的损伤程度，TUNEL检测小肠上皮细胞的凋亡。部分小肠组织用来检测丙二醛、超氧化物歧化酶及激活型caspase-3的表达水平。结果： 乳果糖预处理显著减轻缺血再灌注引起的肠组织损伤和小肠上皮细胞凋亡，并显著抑制血清中细胞因子的水平和肠组织的脂质过氧化。结论： 乳果糖预处理可能通过抑制细胞凋亡和脂质过氧化减轻缺血再灌注引起的肠道损伤。

The protective effect of lactulose pre-treatment against intestinal ischemia reperfusion injury

Objective To investigate the protective effect of lactulose pre-treatment on intestinal ischemia reperfusion． Method 30 Sprague-Dawley rats were divided randomly into three groups: sham-operated, IR and IR plus lactulose pre-treatment. Lactulose (0.1g/ml, 1ml/100g) was administered in the lactulose group, via gavage 7 days prior to operation, and equal volume of saline was administered in the other two groups. Intestinal I/R injury was induced in the groups of I/R and lactulose using bulldog clamps in superior mesenteric artery by 30 min ischemia followed by 60min reperfusion. Following reperfusion, serum samples were collected for estimation of IL-6,TNF-α and IL-1β. Segments of terminal jejunum were rapidly fixed in 4% PFA, and HE staining was used to assess the histopathology. Apoptosis in intestinal epithelium was determined with terminal deoxynucleotidyl transferase dUTP nick end labeling technique (TUNEL). Samples of terminal jejunum were also taken for measuring malondialdehyde，superoxide dismutase and the expression of cleaved caspase3. Result Lactulose pre-treatment significantly attenuated the severity of intestinal I/R injury, with inhibition of IR induced apoptosis. Moreover, lactulose pre-treatment significantly limited the release of inflammation factor and lipid oxidation. Conclusions These results suggest that lactulose pre-treatment has a protective effect against intestinal ischemia reperfusion. This protective effect is possibly due to its ability to inhibit IR-induced apoptosis and oxidative stress.