脂多糖促进小肠缺血再灌注损伤的机制探讨  

Intestinal ischemia reperfusion injury induced by lipopolysaccharide

作　　者：沈晓菲[1] 赵阳[2] 陈辉[2] 赵勇[2] 杜峻峰[3] 管文贤[1] 

机构地区：[1]南京医科大学附属鼓楼临床医学院普通外科,南京210008 [2]中国科学院动物研究所生物膜与膜生物国家重点实验室 [3]北京军区总医院普通外科

出　　处：《中华普外科手术学杂志（电子版）》2013年第3期51-54,共4页Chinese Journal of Operative Procedures of General Surgery(Electronic Edition)

基　　金：国家自然科学基金资助项目(81000189)

摘　　要：目的观察脂多糖(LPS)处理对于小肠缺血再灌注损伤(IRI)的影响及其机制的初步探讨。方法实验分为3组:LPS组(腹腔注射LPS100μg/只)、缺血再灌注(I/R)组(肠系膜上动脉夹闭30min后恢复血供)以及LPS+I/R组(肠系膜上动脉夹闭30min后恢复血供,并立即给予腹腔注射LPS100μg/只),于再灌注后各时间点,获取全小肠,留取病理组织,并分离黏膜固有层细胞,提取总RNA,通过实时荧光定量RT-PCR检测各炎性细胞因子mRNA的表达水平。结果与I/R组、LPS组比较,I/R+LPS组小鼠小肠黏膜固有层各主要细胞炎性因子呈现提前上调表达趋势,病理结果证实再灌注后48h,I/R+LPS组较之I/R组和LPS组小肠损伤显著加重。再灌注后48h结果显示,与I/R组比较,LPS组IL-17AmRNA水平无显著变化[(6.20±0.32)与(5.79±0.30),t=3.117,P>0.05];而LPS+I/R组与其余两组相比,IL-17AmRNA表达水平均明显上调[(14.22±0.5)与(6.20±0.32),t=59.047,P<0.05],[(14.22±0.5)与(5.79±0.30),t=134.754,P<0.05],其差异有统计学意义。结论小肠缺血后外源性LPS可加速并加重再灌注损伤,这可能与IL-17A表达上调,促进相关免疫细胞浸润有关。Obejectives To investigate the effects of lipopolysaccharide （LPS） treatment on intestinal ischemia reperfusion injury and its mechanisms. Methods Mice were assigned randomly into an LPS treatment group （ 100 p.g LPS per mouse, i. p. ） ; an ischemia reperfusion group （ occlusion of the superior mensenteric artery for 30 minutes, followed by reperfusion） ; and an LPS ＋ I/R group （ occlusion of the superior mensenterie artery for 30 minutes, followed by reperfusion and 100 p.g LPS per mouse i. p. ）. The whole small intestine of the mice was harvested at individual time point after repeffusion, and pathological examination was performed. Total RNA of isolated lymphocytes from the intestinal lamina propria was extracted, and mRNA expression of each proinflammatory cytokine was detected by real-time RT PCR. Results Compared to the LPS treatment group and the ischemia reperfusion group, mRNA expression of proinflammatory eytokines exhibited an accelerated trend in the LPS ＋ I/R group. These results were further confirmed by pathological results showing that the intestinal injury in the LPS ＋ I/R group was severer 48 hours post-reperfusion. There was no significant difference in the mRNA level of IL-17A between the LPS treatment group and the I/R group at the time point of 48 hours E （ 6.20 ±0.32 ） vs. （ 5.79 ±0.30 ）, t=3. 117, P〉0.05]; whereas compared to the other two groups, the mRNA level of IL-17A was significantly increased in the LPS ＋ I/R group E （ 14.22± 0. 5 ） vs. （ 6.20±0.32 ）, t = 59. 047, P 〈 0. 05 ], I （ 14.22 ± 0.5 ） vs. （ 5.79± 0. 30 ）, t = 134. 754, P 〈 0. 05 ]. Conclusion Intestinal ischemia reperfusion injury could be accelerated by exogenous LPS treatment, which might be mediated by IL-17A-producing infiltrated immunocytes.

关 键 词：脂多糖类 小肠 再灌注损伤 白细胞介素17 动物实验 

分 类 号：R656.7[医药卫生—外科学]