文章摘要
陈兆红华青△ 舒志荣赵园园马凯徐以凤王甜甜.IL-10 在单纯疱疹病毒性脑炎小鼠脑中的表达及其机制的研究[J].,2012,12(9):1628-1631
IL-10 在单纯疱疹病毒性脑炎小鼠脑中的表达及其机制的研究
The Study of IL-10 Expression and Immunologic Mechanism in the BrainTissue of Mice with Herpes Simplex Virus Encephalitis
  
DOI:
中文关键词: 单纯疱疹病毒性脑炎  阿昔洛韦  糖皮质激素  IL-10
英文关键词: Herpes simplex encephalitis  Acyclovir  Glucocorticoid  IL-10
基金项目:青岛市科技局项目(07-2-1-17-nsh-1)
作者单位
陈兆红华青△ 舒志荣赵园园马凯徐以凤王甜甜 青岛大学医学院附属医院 
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中文摘要:
      目的:研究在单纯疱疹病毒性脑炎小鼠脑组织中IL-10 的表达并探讨其可能的免疫学机制。方法:小鼠被随机分为四组,每 组7 只:空白对照组, 病毒感染组,阿昔洛韦组和地塞米松组。后3 组的小鼠被接种HSV-1 病毒液制造单纯疱疹脑炎模型。我们用 免疫组化的方法比较各组脑炎小鼠脑组织中IL-10 的表达。观察小鼠神经损伤的表现,行神经症状评分。并采用Pearson 相关分析 神经症状评分与IL-10 表达的相关性。结果:病毒感染组神经损伤最重,神经症状评分最高,阿昔洛韦组次之,地塞米松组最低 (P<0.05)。IL-10 在HSE 小鼠脑组织中的表达较正常对照组明显上调(P<0.05),病毒感染组较阿昔洛韦组高(P<0.05),病毒感染组 和阿昔洛韦组较地塞米松组增高(P<0.05)。神经症状评分与IL-10 的表达呈正相关(r=0.82, P<0.05)。结论:IL-10 可能抑制小胶质 细胞炎性因子的产生,减轻神经细胞的损伤等介导宿主在HSE 中的免疫应答作用。
英文摘要:
      Objective: To investigate the IL-10 expression in the brain tissue of mice with herpes simplex encephalitis and the possible immunologic mechanism. Methods: Mice were randomly divided into 4 groups with 7 mice in each: normal control group, HSV-1 infection group, acyclovir treated group, and dexamethasone treated group. The mice in last three groups were inoculated with HSV-1 solution to make the models of HSE. The expressions of IL-10 of the mice brain tissues in each group were compared by using immunohistochemisty. The mice were observed carefully and the score of neurological injury of the mice was assessed. Pearson Correlations was used to describe the correlations of cytokines and neurological injury score. Results: The neurological injury score was the highest in HSV-1 infection group than that in the other groups, and the dexamethasone treated group was the lowest than others (P<0.05). The neurological injury score in acyclovir treated group was between the scores in HSV-1 infection group and dexamethasone treated group. After HSV-1 infection, IL-10 was significantly increased compared with that in normal control group (P<0.05). The production of IL-10 in acyclovir treated group decreased compared with HSV-1 infection group (P<0.05), and examethasone treated group decreased significantly compared with that in HSV-1 infection group and acyclovir treated group (P<0.05). IL-10 and neurological injury score were positive correlation (r=0.82, P<0.05). Conclusions: IL-10 may inhibit the production of inflammatory cytokines by microglia and protect CNS against the immune injury to regulate the size of the immune response.
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