氧化应激在脓毒症所致胃肠动力障碍中的作用机制及厚朴酚干预作用的实验研究  

Magnolol Pretreatment Prevents from Sepsis-induced Intestinal Dysmotility by Corrective Oxidative Stress

作　　者：苗彬[1] 张淑文[1] 王红[1] 齐文杰[1] 王超[1] 胡岚[1] 黄光伟[1] 

机构地区：[1]首都医科大学附属北京友谊医院感染内科,北京100050

出　　处：《中国中西医结合外科杂志》2015年第4期369-372,共4页Chinese Journal of Surgery of Integrated Traditional and Western Medicine

基　　金：国家自然科学基金(81173411);北京市科技计划(Z141100002114004);北京市自然科学基金(7152044)

摘　　要：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(i NOS)m RNA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i NOS m RNA的表达较对照组显著增强。结论:过度氧化应激、i NOS m RNA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。Objective To investigate the mechanism by which magnolol treatment prevents from sepsis-induced dysmotility in LPS-treated mice and role of oxidative stress. Methods Sepsis was induced by intravenous 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 malondialdehyde （MDA） concentration were detected using commercial kits. Results Intestinal transit and muscular contractility 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 contraction （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 reduced 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, iNOS expression, and MDA concentration, and decrease in SOD activity in LPS-treated animals （P〈0.05）. Conclusion The laboratory results suggested that magnolol treatment can prevent from sepsis-induced intestinal dysmotility by regulating oxidative stress.

关 键 词：脓毒症 胃肠功能障碍 厚朴酚 氧化应激 

分 类 号：Q95-33[生物学—动物学] R631[医药卫生—外科学]