脓毒症大鼠小肠动力障碍及厚朴酚干预实验研究

doi:10.3969/j.issn.1006-7795.2009.06.029

首都医科大学学报 ›› 2009, Vol. 30 ›› Issue (6): 849-853.doi: 10.3969/j.issn.1006-7795.2009.06.029

脓毒症大鼠小肠动力障碍及厚朴酚干预实验研究

杨铁城¹, 张淑文², 王红², 任添华¹

1. 首都医科大学附属北京天坛医院急诊科;2. 首都医科大学附属北京友谊医院感染内科

收稿日期:2009-05-26 修回日期:1900-01-01 出版日期:2009-12-21 发布日期:2009-12-21
通讯作者: 任添华

Magnolol Attenuats Sepsis-induced Gastrointestinal Dysmotility in Rats

YANG Tie-cheng¹, ZHANG Shu-wen², WANG Hong², REN Tian-hua¹

1. Department of Emergency, Beijing Tiantan Hospital, Capital Medical University;2. Department of Infection, Beijing Friendship Hospital, Capital Medical University

Received:2009-05-26 Revised:1900-01-01 Online:2009-12-21 Published:2009-12-21

摘要/Abstract

摘要： 目的观察厚朴酚对于脓毒症大鼠肠动力学的影响并探讨其作用机制。方法采用腹腔注射内毒素(lipopolysaccharide,LPS)的方法制备脓毒症大鼠模型, 厚朴酚(10^-5 g/kg)于注射内毒素前15 min尾静脉注射。按随机数字表法将动物随机分为3组,分别为模型干预组、模型安慰剂组和对照安慰剂组,于造模12 h后测定各组动物小肠传输百分率和离体肌条肌张力。同时测定小肠组织一氧化氮(NO)含量。另外,于造模后2 h测定小肠肌条组织诱导型一氧化氮合酶(inducible nitric oxide synthase,iNOS)mRNA的表达水平,同时测定超氧化物歧化酶(superoxide dismutase,SOD )活力以及丙二醛(malondialdehyde,MDA)含量。结果厚朴酚可以明显增加脓毒症大鼠小肠传输速率(P=0.002),明显增加脓毒症大鼠小肠肌条自主收缩频率以及小肠肌条对于甲酰甲胆碱机械收缩反应。厚朴酚能够明显下调脓毒症大鼠iNOSmRNA的表达(P=0.000),降低脓毒症大鼠小肠组织NO含量(P<0.01)。另外厚朴酚可以增加脓毒症大鼠小肠组织SOD活力,减少MDA含量(P=0.000)。结论厚朴酚预处理可以显著改善脓毒症大鼠的小肠动力障碍。拮抗氧化应激和降低NO合成可能是其产生这一有益作用的主要机制。

关键词: 脓毒症, 厚朴酚, 内毒素, 一氧化氮

Abstract: Objective To investigate the protective effects of magnolol against sepsis-induced inflammation and intestinal dysmotility. Methods Sepsis was induced by a single intraperitoneal injection of lipopolysaccharide(LPS). Male Wistar rats were randomly assigned to one of three treatment groups: magnolol before LPS injection(LPS/Mag group); vehicle before LPS injection(LPS/Veh group); and vehicle before injection of saline(Control/Veh) group. Intestinal transit and ex vivo circular intestinal muscle mechanical activity were assessed 12 h after LPS injection. Inducible nitric oxide synthase(iNOS) mRNA in rat intestine was studied by RT-PCR 2 h after LPS injection. In addition, antioxidant activity was determined by measuring malondialdehyde(MDA) concentration and superoxide dismutase(SOD) activity in the intestine 2 h after LPS injection. Nitrogen monoxide(NO) concentration in the intestine was also measured 12 h after LPS injection. Results Magnolol significantly increased the intestinal transit and circular muscle mechanical activity in LPS-treated animals. The iNOS mRNA expression in the small intestine were significantly reduced after magnolol treatment in LPS-induced septic animals. Moreover, magnolol significantly decreased MDA concentration and increased SOD activity in the rat intestine. Magnolol also significantly decreased NO concentration in the septic rat intestine 12 h after LPS injection. Conclusion Magnolol prevented sepsis-induced suppression of intestinal motility. The potential mechanism of this benefit of magnolol appears to be associated with blocking oxidative stress and decreasing the production of NO in the intestine.

Key words: sepsis, magnolol, lipopolysaccharide, nitrogen monoxidum

中图分类号:

R 453

杨铁城;张淑文;王红;任添华. 脓毒症大鼠小肠动力障碍及厚朴酚干预实验研究[J]. 首都医科大学学报, 2009, 30(6): 849-853.

YANG Tie-cheng;ZHANG Shu-wen;WANG Hong;REN Tian-hua. Magnolol Attenuats Sepsis-induced Gastrointestinal Dysmotility in Rats[J]. Journal of Capital Medical University, 2009, 30(6): 849-853.

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脓毒症大鼠小肠动力障碍及厚朴酚干预实验研究

Magnolol Attenuats Sepsis-induced Gastrointestinal Dysmotility in Rats

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