摘要
为确定紫锥菊多糖对内毒素血症小鼠炎症反应的保护作用,将100只BALB/c小鼠随机分成正常组,模型组,紫锥菊多糖高、中、低剂量组(分别为2.0,1.0,0.5 g/kg),每组20只。模型组、紫锥菊多糖各组小鼠通过腹腔注射脂多糖(8 mg/kg)造模,正常组小鼠腹腔注射等量生理盐水。紫锥菊多糖分别于造模前灌胃给药5次(间隔24 h)并在造模后持续给药2次(间隔24 h);正常组和模型组小鼠只灌服等体积生理盐水。各实验组小鼠分别于造模后1,6,24,48 h剖杀,ELISA法检测血清中的肿瘤坏死因子(tumor necrosis factor-α,TNF-α)、白细胞介素-1β(Interleukin-1β,IL-1β)、白细胞介素-6(Interleukin-6,IL-6)的浓度和肺脏组织的湿质量/干质量值。结果表明:紫锥菊多糖组小鼠的血清中TNF-α,IL-1β,IL-6浓度明显低于模型组(P<0.05),肺脏组织的湿质量/干质量值明显低于模型组(P<0.05),且紫锥菊多糖高剂量组小鼠的效果最好。因此,紫锥菊多糖能够为内毒素血症小鼠炎症提供保护作用。
This paper is to study the inflammation protection of Echinacea purpurea in endotoxemia mice. 100 Balb / c mice were randomly divided into normal group and model group,echinacea high,medium and low dose( 2. 0,1. 0,0. 5 g / kg) group,twenty mice for each group. Model group and echinacea purpurea polysaccharide group mice were induced by abdominal cavity injection of endotoxin( 8 mg / kg). Normal group mice were injected equal volume physiological saline. Before establishment of the mice model,Echinacea purpurea polysaccharide group mice were filled the stomach five times before the model and two times after the model( interval 24 h). Normal group and endotoxemia group mice were filled the stomach equal volume physiological saline. The mice were killed after establishment of the mice model on 1,6,24,48 hour. Cytokines of TNF-α,IL-1β and IL-6 were detected by ELISA. In addition,the proportion of wet wight / dry wight in lung tissue were detected. Results showed that concentration of TNF-α,IL-1β,IL-6 and the proportion of wet wight / dry wight in endotoxemia mice increased significantly than the other group. Echinacea purpurea can protect the inflammation of endotoxemia mice.
出处
《河北科技师范学院学报》
CAS
2015年第3期8-11,共4页
Journal of Hebei Normal University of Science & Technology
基金
国家自然科学基金资助项目(项目编号:31472230)
河北省自然科学基金资助项目(项目编号:C2014407068)
河北省科技厅科技支撑计划项目(项目编号:14966610D
12220408D)
石家庄市科技局科技支撑计划项目(项目编号:131200063A)
河北省教育厅百名优秀创新人才支持计划(Ⅱ)项目(项目编号:ZH2011244
Q2012037)
关键词
紫锥菊
内毒素血症
肿瘤坏死因子
白细胞介素
Echinacea purpurea Polysaccharide
endotoxemia
tumor necrosis factor
interleukin