CAJ | 학술논문

目的：研究氧化应激在脓毒症所致胃肠运动障碍小鼠模型中的作用机制以及厚朴酚对其干预作用。方法：采用尾静脉注射内毒素（LPS）的方法制备脓毒症所致胃肠运动障碍小鼠模型。60只小鼠随机分为4组，对照组、模型组、厚朴酚干预组和莫沙必利干预组。厚朴酚干预组在注射LPS后30 min尾静脉注射厚朴酚15μg/kg。莫沙必利干预组则以相同方式注射莫沙必利1.5 mg/kg。造模后12 h分别测定各组小肠传输速率、小肠平滑肌肌条自主收缩频率以及波幅。提取小肠肌条组织测定超氧化物歧化酶（SOD）活力、丙二醛（MDA）和一氧化氮（NO）含量。并以RT-PCR法测定分泌型一氧化氮合酶（iNOS）mRNA表达。结果：造模12 h后，脓毒症模型组小肠传输速率和小肠肌条自主收缩频率和波长较对照组明显减慢（P＜0.05），厚朴酚和莫沙必利干预可以明显增加小肠传输速率（P＜0.05），并且明显增加小肠肌条收缩频率和波长（P＜0.05）。与对照组相比，模型组小肠组织SOD活力明显降低（P＜0.05），MDA和NO水平显著增高（P＜0.05），提示脓毒症时小肠处于过度氧化应激状态。RT-PCR结果显示注射LPS后0.5 h大鼠小肠组织iNOS mRNA的表达较对照组显著增强。结论：过度氧化应激、iNOS mRNA表达抑制是脓毒症所致胃肠运动障碍的重要发生机制。厚朴酚可以改善脓毒症所致胃肠运动障碍。拮抗氧化应激可能是其产生这一作用的机制。
목적：연구양화응격재농독증소치위장운동장애소서모형중적작용궤제이급후박분대기간예작용。방법：채용미정맥주사내독소（LPS）적방법제비농독증소치위장운동장애소서모형。60지소서수궤분위4조，대조조、모형조、후박분간예조화막사필리간예조。후박분간예조재주사LPS후30 min미정맥주사후박분15μg/kg。막사필리간예조칙이상동방식주사막사필리1.5 mg/kg。조모후12 h분별측정각조소장전수속솔、소장평활기기조자주수축빈솔이급파폭。제취소장기조조직측정초양화물기화매（SOD）활력、병이철（MDA）화일양화담（NO）함량。병이RT-PCR법측정분비형일양화담합매（iNOS）mRNA표체。결과：조모12 h후，농독증모형조소장전수속솔화소장기조자주수축빈솔화파장교대조조명현감만（P＜0.05），후박분화막사필리간예가이명현증가소장전수속솔（P＜0.05），병차명현증가소장기조수축빈솔화파장（P＜0.05）。여대조조상비，모형조소장조직SOD활력명현강저（P＜0.05），MDA화NO수평현저증고（P＜0.05），제시농독증시소장처우과도양화응격상태。RT-PCR결과현시주사LPS후0.5 h대서소장조직iNOS mRNA적표체교대조조현저증강。결론：과도양화응격、iNOS mRNA표체억제시농독증소치위장운동장애적중요발생궤제。후박분가이개선농독증소치위장운동장애。길항양화응격가능시기산생저일작용적궤제。
Objective To investigate the mechanism by which magnolol treatment prevents from sepsis-in?duced dysmotility in LPS-treated mice and role of oxidative stress. Methods Sepsis was induced by intrave?nous tail vein injection of LPS. Sixty mice were divided into four groups: the magnolol-treated septic group, the mosapride-treated septic group,the placebo-treated septic group, and the placebo-treated sham-operated group. Intestinal transit and circular smooth muscle contraction were measured 12 h after LPS injection, and the mRNA levels of iNOS were determined by RT-PCR. NO content, superoxide dismutase (SOD) activity, and malondialde?hyde (MDA) concentration were detected using commercial kits. Results Intestinal transit and muscular con?tractility were significantly lower in the LPS-treated group than in the control group. In LPS-treated animals, magnolol pretreatment significantly accelerated intestinal transit (P<0.05), increased circular muscle contrac?tion (P<0.05). In addition, NO concentration and iNOS expression were significantly increased in the LPS-treated group compared with the control group (P<0.05). Furthermore, SOD activity was significantly re?duced and MDA concentration was significantly increased in the LPS-treated group compared with the control group (P<0.05). Magnolol pretreatment prevented the sepsis-induced increase in NO concentration, iN?OS expression, and MDA concentration, and de?crease in SOD activity in LPS-treated animals (P<0.05). Conclusion The laboratory results suggest?ed that magnolol treatment can prevent from sep?sis-induced intestinal dysmotility by regulating oxidative stress.