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作 者:刘丹[1] 王莉新[1] 杨秋美[1] 缪珠雷[1] 陈圣敏[2] 王易[1]
机构地区:[1]上海中医药大学免疫学与病原生物学教研室,上海201203 [2]上海中医药大学教学实验中心,上海201203
出 处:《现代免疫学》2010年第2期142-146,共5页Current Immunology
基 金:上海高校选拔培养优秀青年教师科研专项基金;上海市教委高水平特色发展项目[沪教委财(2005)81号];上海市教委重点学科建设资助项目(J5030)
摘 要:通过利什曼原虫感染模型,探讨中药复方加味玉屏风散对感染机体免疫调节机制的影响。选用加味玉屏风散及其单味主药对利什曼原虫感染模型进行干预。RT-PCR法检测脾细胞内细胞因子IFN-γ和IL-4 mRNA表达水平,反映感染模型内Th1/Th2平衡状态;流式细胞仪分析脾脏内CD4^+CD25^+Treg(Treg)水平。与正常对照鼠相比较,利什曼原虫感染BALB/c小鼠脾脏内存在IL-4表达增强,呈Th2偏离;且其脾细胞内Treg水平显著升高(P<0.05),加味玉屏风散复方或其单味主药可以下调感染动物脾脏内Treg水平(P<0.05),下调脾细胞IL-4表达(P<0.05),抑制感染部位的肿胀程度(P<0.05),减轻病变。利什曼原虫感染动物模型存在免疫偏离,呈Th2优势应答,且存在Treg水平的增加,二个因素共同作用可能成为易感动物感染持续存在原因;加味玉屏风散复方及主药可以显著下调感染机体内Treg水平,直接或间接抑制Th2优势应答的免疫偏离状态,从而实现抗感染的效力。To explore the potential effect of the Chinese herb compound modified Yu Ping Feng pulvis (MYP) on the immunoregulatory mechanism in mouse model of Leishumania infection, the main single component of herb medicine was used and the expression level of the intracellular cytokines was analyzed by RT-PCR to reflect the status of Th1/Th2 imbalance in this infeetion model. Meanwhile, the level of the CD4+ CD25+ regulatory T cells (Tregs) in spleen of the infected mice was determined by FACS. Compared with the control mice, the level of Tregs increased remarkahly (P〈0.05), while the expression of IL-4 was increased in the Leishrnania infected mice, showing a dominant Th2 response. MYP or it's single component could downregulate the level of Tregs and the expression level of IL-4 (P〈0. 05) in the infectious model, and inhibited the degree of swelling at the infected sites (P〈0.05) as well as the development of infection. It was shown that the Leishrnania infected mice was in the immune deviation state with a dominant Th2 response and the elevated level of the Tregs. These results suggest that the co-existence of these two factors mentioned might be the cause of persistence of infection in the susceptible animals. Traditional Chinese herb medicine MYP compound and or it's main single components can suppress the level of Tregs markedly and modulate the immune deviation inclining to dominant Th2 response in infectious model, thereby inhibiting the development of infection.
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