Abstract:

Objective To elucidate the role of mast cells（MC）activation in the jejunal mucous membrane in the pathogene? sis of cryptosporidiosis（CPS）and explore the mechanism of prevention and treatment of radix sophorae flavescetis （RSF）mixture on CPS. Methods A total of 30 healthy male BALB/c mice were randomly divided into a normal control group，CPS model con? trol group and RSF mixture experimental group. The mice of CPS model were inoculated intragastrically with 1×105 Cryptosporidi? um oocyst （CSO） . The mice in the RSF mixture experimental group were treated with inoculation of RSF mixture（0.2 ml doses） twice one week for three weeks continuously after CPS models were established. Pathological changes of the jejunal mucosa mem? brane were observed by a light microscope. The MCs were stained by toluidine blue，the number of mast cells was recorded and the changes of degranulation were observed. Results The HE staining showed inflammatory pathological changes in the jejunal muco? sa membrane of the CPS model control group. After three?week treatment of RSF mixture，the small intestine epithelium was inte? grated on the whole. The toluidine blue stain showed the number of mast cell in submucosa and muscular layer of the jejunal mu? cous membrane increased significantly in the model control group（12.80±0.84）compared with those of the normal control group （1.60±0.89） （P <0.01）and an obvious degranulation was seen in the CPS model control group. The number of mast cells of the mice in the RSF mixture experimental group decreased significantly（P < 0.01）and the number（2.00±0.71）and morphous were closed to the normal after administration for three weeks. Conclusions MC activation is involved in the intestinal inflammatory re? sponse caused by Cryptosporidium. RSF mixture could decline the number of MC，inhibit the activation and degranulation of MC in the jejunal mucosa membrane of CPS mice to reduce inflammation and repair the damaged intestinal mucosa，which may realize the purpose of treatment of CPS.

Key words: Cryptosporidium；BALB/c mice；Radix sophorae flavescentis mixture；Mast cell； Mouse

摘要：

目的 阐明空肠黏膜肥大细胞激活在隐孢子虫致病机制中的作用， 探讨苦参合剂抗隐孢子虫感染的作用机理。方法 30只雄性BALB/c小鼠随机分为正常对照组、 隐孢子虫感染模型对照组和苦参合剂实验组。建立隐孢子虫肠道感染小鼠模型， 经苦参合剂治疗3周后， 光镜下观察小鼠空肠病理变化； 甲苯胺蓝染色， 计数肥大细胞数量并观察其脱颗粒变化。结果 隐孢子虫感染模型对照组小鼠小肠上皮出现明显炎性病理改变。苦参合剂实验组小鼠治疗3周后小肠上皮较完整， 接近正常。甲苯胺蓝染色显示隐孢子虫感染模型对照组小鼠肥大细胞数量 （12.80±0.84） 较正常对照组 （1.60±0.89）明显增多 （P < 0.01）， 且脱颗粒现象明显； 苦参合剂实验组小鼠肥大细胞数量 （2.00±0.71） 较隐孢子虫感染模型组明显减少（P < 0.01）， 肥大细胞数量和形态接近正常对照组。结论 肥大细胞活化参与了隐孢子虫感染引起的肠黏膜炎症反应。苦参合剂可减少隐孢子虫感染小鼠空肠黏膜肥大细胞数量及抑制肥大细胞活化脱颗粒， 从而减轻炎症、 修复受损肠黏膜， 发挥治疗隐孢子虫病的作用。

关键词: 隐孢子虫； 苦参合剂； 肥大细胞； 小鼠