目的:观察蒲公英多糖(dandelion polysaccharide,DP)对大鼠多器官功能障碍综合征(multiple organ dysfunction syndrome,MODS)肺、小肠组织炎症反应及S100钙结合蛋白A8/A9(S100 calcium-binding protein A8/A9,S100A8/A9)表达的影响。方...目的:观察蒲公英多糖(dandelion polysaccharide,DP)对大鼠多器官功能障碍综合征(multiple organ dysfunction syndrome,MODS)肺、小肠组织炎症反应及S100钙结合蛋白A8/A9(S100 calcium-binding protein A8/A9,S100A8/A9)表达的影响。方法:应用失血性休克及腹腔注射脂多糖“二次打击”的方法,构建大鼠MODS模型,分为假手术组、模型组、DP低剂量组、DP高剂量组。观察各组大鼠肺和小肠脏器系数及湿/干重比值;苏木精-伊红(hematoxylin-eosinstaining,HE)染色观察肺和小肠组织病理形态学改变;免疫组织化学染色观察肺和小肠组织白细胞介素(interleukin,IL)1β、IL-6、IL-10的表达;蛋白质免疫印迹法(Western blot)检测肺和小肠组织S100A8/A9蛋白表达变化。结果:与假手术组相比,模型组大鼠肺脏系数(5.849±0.824)、湿/干重比值(6.556±0.631)和小肠湿/干重比值(6.356±0.535)、湿重/长度比值(73.950±5.569)均上升。HE染色显示肺泡腔及肺间质可见大量炎细胞浸润,肺泡壁增厚;小肠绒毛崩解碎裂,可见炎细胞浸润及节段性集合淋巴滤泡增生。S100A8/A9主要表达于中性粒细胞和巨噬细胞,大鼠肺和小肠组织S100A8/A9、IL-1β、IL-6表达上调,IL-10表达下调。给予高剂量DP治疗后,大鼠肺脏系数(4.297±0.462)、湿/干重比值(5.313±0.495)和小肠湿/干重比值(5.398±0.388)、湿重/长度比值(59.417±2.891)均下降。肺和小肠组织病理损伤减轻,肺和小肠组织S100A8/A9、IL-1β、IL-6表达下调,IL-10表达上调。结论:DP可能通过抑制S100A8/A9的表达,减轻大鼠MODS肺和小肠组织损伤的炎症反应。展开更多
Systemic inflammatory response syndrome (SIRS) and its lethal sequela multiple organ dysfunction syndrome (MODS) are common complications in critical illness, such as severe trauma, shock, infection and major operatio...Systemic inflammatory response syndrome (SIRS) and its lethal sequela multiple organ dysfunction syndrome (MODS) are common complications in critical illness, such as severe trauma, shock, infection and major operations. During the past three decades, the evolution in our understanding of SIRS and/or MODS could be divided into three stages. Particularly in recent years, advances in molecular and cellular biology have provided new insights in the pathogenesis of this complex condition. The earlier emphasis on the pro inflammatory mediators involved in propagation of inflammatory response, has gradually been replaced by a realization that SIRS/MODS are the result of an imbalance of pro and anti inflammatory mediators to create the final status of excessive inflammation or immunoparalysis’. Though prognosis remains poor, the knowledge that now exists about SIRS/MODS gives great hope for the future. Progress has been made in new treatment modalities and re evaluation of current available measures. Nevertheless, improved techniques to monitor immunological or other markers of inflammatory and host defense responses will be important in assessing the effects of future therapies on central mechanisms contributing to SIRS/MODS.展开更多
文摘目的:观察蒲公英多糖(dandelion polysaccharide,DP)对大鼠多器官功能障碍综合征(multiple organ dysfunction syndrome,MODS)肺、小肠组织炎症反应及S100钙结合蛋白A8/A9(S100 calcium-binding protein A8/A9,S100A8/A9)表达的影响。方法:应用失血性休克及腹腔注射脂多糖“二次打击”的方法,构建大鼠MODS模型,分为假手术组、模型组、DP低剂量组、DP高剂量组。观察各组大鼠肺和小肠脏器系数及湿/干重比值;苏木精-伊红(hematoxylin-eosinstaining,HE)染色观察肺和小肠组织病理形态学改变;免疫组织化学染色观察肺和小肠组织白细胞介素(interleukin,IL)1β、IL-6、IL-10的表达;蛋白质免疫印迹法(Western blot)检测肺和小肠组织S100A8/A9蛋白表达变化。结果:与假手术组相比,模型组大鼠肺脏系数(5.849±0.824)、湿/干重比值(6.556±0.631)和小肠湿/干重比值(6.356±0.535)、湿重/长度比值(73.950±5.569)均上升。HE染色显示肺泡腔及肺间质可见大量炎细胞浸润,肺泡壁增厚;小肠绒毛崩解碎裂,可见炎细胞浸润及节段性集合淋巴滤泡增生。S100A8/A9主要表达于中性粒细胞和巨噬细胞,大鼠肺和小肠组织S100A8/A9、IL-1β、IL-6表达上调,IL-10表达下调。给予高剂量DP治疗后,大鼠肺脏系数(4.297±0.462)、湿/干重比值(5.313±0.495)和小肠湿/干重比值(5.398±0.388)、湿重/长度比值(59.417±2.891)均下降。肺和小肠组织病理损伤减轻,肺和小肠组织S100A8/A9、IL-1β、IL-6表达下调,IL-10表达上调。结论:DP可能通过抑制S100A8/A9的表达,减轻大鼠MODS肺和小肠组织损伤的炎症反应。
文摘Systemic inflammatory response syndrome (SIRS) and its lethal sequela multiple organ dysfunction syndrome (MODS) are common complications in critical illness, such as severe trauma, shock, infection and major operations. During the past three decades, the evolution in our understanding of SIRS and/or MODS could be divided into three stages. Particularly in recent years, advances in molecular and cellular biology have provided new insights in the pathogenesis of this complex condition. The earlier emphasis on the pro inflammatory mediators involved in propagation of inflammatory response, has gradually been replaced by a realization that SIRS/MODS are the result of an imbalance of pro and anti inflammatory mediators to create the final status of excessive inflammation or immunoparalysis’. Though prognosis remains poor, the knowledge that now exists about SIRS/MODS gives great hope for the future. Progress has been made in new treatment modalities and re evaluation of current available measures. Nevertheless, improved techniques to monitor immunological or other markers of inflammatory and host defense responses will be important in assessing the effects of future therapies on central mechanisms contributing to SIRS/MODS.
