%0 Journal Article %T 右美托咪定对脓毒症大鼠肺组织髓样细胞触发受体-1表达的影响<br>Effect of dexmedetomidine on expression of triggering receptor expressed on myeloid cells-1 in lung tissues of rats with sepsis %A 陆洋 %A 薛飞 %A 赵宏胜 %A 等< %A br> %A LU Yang %A XUE Fei %A ZHAO Hong-sheng %A et al %J 上海交通大学学报（医学版） %D 2015 %R 10.3969/j.issn.1674-8115.2015.09.007 %X 目的 观察右美托咪定对脓毒症大鼠肺髓样细胞触发受体-1 （TREM-1）表达的影响。方法 将60只雄性SD大鼠随机分为假手术组（n=15）、脓毒症对照组（n=15）、脓毒症右美托咪定组（n=15）和脓毒症育亨宾+右美托咪定组（n=15）。通过盲肠结扎穿孔法（CLP）建立脓毒症模型，观察各组的24 h生存率；采用ELISA法测定血清白介素-6（IL-6）、肿瘤坏死因子-α（TNF-α）和可溶性TREM-1（sTREM-1）浓度；观察肺组织病理变化并进行评分，通过real-time PCR和免疫组织化学法测定大鼠肺组织TREM-1的表达水平。结果 与脓毒症对照组相比，右美托咪定组死亡率及血清IL-6、TNF-α和sTREM-1浓度明显下降（P<0.05）；肺组织炎症反应明显减轻（P<0.05）；TREM-1的表达明显下降（P<0.05）。结论 右美托咪定可通过抑制TREM-1的表达而减轻脓毒症大鼠肺部的炎症反应。<br>： Objective To observe the effect of dexmedetomidine on the expression of triggering receptor expressed on myeloid cells-1 (TREM-1) in lung tissues of rats with sepsis. Methods Sixty male Sprague Dawley (SD) rats were randomly divided into the sham group (n=15), sepsis group (n=15), dexmedetomidine group (n=15), and yohimbine+ dexmedetomidine group (n=15). The sepsis model was established by cecal ligation and puncture (CLP). The survival rate of rats in 24 h was observed. Serum IL-6, TNF-α, and sTREM-1 levels were measured by enzyme-linked immunosorbent assay (ELISA). The pathological changes of lung tissues were observed and scored. The expression of TREM-1 in lung tissues was detected by real-time PCR and immunohistochemichal method. Results Compared with the sepsis group, the mortality rate and serum IL-6, TNF-α, and sTREM-1 levels of dexmedetomidine group remarkably decreased (P<0.05). The inflammatory response of lung tissue significantly alleviated (P<0.05) and the expression of TREM-1 remarkably decreased (P<0.05). Conclusion Dexmedetomidine can alleviate the inflammatory response of lung tissues of rats with sepsis by inhibiting the expression of TREM-1 %K 右美托咪定 %K 髓样细胞触发受体-1 %K 脓毒症 %K 炎症反应 %K < %K br> %K dexmedetomidine %K triggering receptor expressed on myeloid cells-1 %K sepsis %K inflammatory %U http://xuebao.shsmu.edu.cn/CN/abstract/abstract10848.shtml