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机构地区:[1]宁夏医科大学附属医院神经内科,银川750004 [2]宁夏颅脑疾病重点实验室-省部共建国家级重点实验室培育基地,银川750004
出 处:《宁夏医科大学学报》2011年第1期7-9,F0002,共4页Journal of Ningxia Medical University
基 金:2007年国家自然科学基金面上项目(30760067);2007年宁夏自然科学基金项目(NZ0790);教育部春晖计划(Z2008-1-75002)
摘 要:目的了解丙型肝炎病毒(HCV)感染小鼠小胶质瘤细胞(BV2)后Th1/Th2类细胞因子的变化,探讨HCV感染后小胶质细胞的免疫分泌效应。方法体外培养BV2细胞,随机分为HCV阳性血清组、正常人血清组、空白对照组。分别作用24h用倒置显微镜观察细胞形态并收集上清液,ELISA法检测上清液中白介素-12(IL-12)、肿瘤坏死因子α(TNF-α)和白介素-6(IL-6)的含量。结果倒置显微镜下观察显示,HCV阳性血清感染后BV2细胞呈圆形,突起变粗短,部分细胞聚集成团。HCV阳性血清感染组TNF-α、IL-12、IL-6含量均高于正常人血清组与空白对照组,差异有统计学意义(P<0.01);正常人血清组和空白对照组差异无统计学意义(P>0.05)。结论 HCV感染BV2细胞后Th1类细胞因子TNF-α、IL-12、和Th2类细胞因子IL-6分泌增强,可能与HCV感染CNS引起的早期炎症损伤有关。Objective To analyze the changes of Thl/Th2 cytokine after mouse microglia(BV2) infected by hepatitis C virus (HCV) , and to investigate the immune secretory function of BV2 cells after central nervous system (CNS) infected by HCV. Methods BV2 cells were cultured in vitro and divided into 3 groups:HCV -positive serum group, normal serum group (negative control) and blank control group. Each group had 20 samples. Supernatant was collected at the 24th hour to detect the level of interleukin - 12 (IL - 12), tumor necrosis factor α ( TNF -α) and interleukin - 6 ( IL - 6) by ELISA , meanwhile the morphology of BV2 cells were observed. Results BV2 cell morphology showed under the inverted microscope: in vitro , BV2 cells were round, cell process became coarsen and short, and some cells, gathered into the conglobation. The level of TNF -α ,IL - 12, IL -6 in the supernatant in the HCV -positive serum group were higher than those in other groups, the difference showed statistical significance( P 〈 0. 01 ) ; The level of IL- 12, TNF -α, IL- 6 in the supernatant had no significant difference between normal serum group and blank control group ( P 〉 0.05 ). Conclusion HCV may induce the secretion of IL- 12,TNF-α,IL- 6 by BV2. The secretion of Thl Cytokines and Th2 Cytokines was increased after HCV infected. It indicated that TNF - α, IL - 12, IL - 6 may be involved in the early inflammatory injury and immune response in CNS infected HCV.
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