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慢病毒介导Fg12基因沉默技术对自身免疫性心肌炎大鼠Th1/Th2漂移及Th17/Treg平衡的影响 被引量:2
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作者 张晶晶 刘婕 +3 位作者 杨占峰 孙岩 岳丽晓 何群力 《中国比较医学杂志》 CAS 北大核心 2020年第7期38-44,共7页
目的探讨慢病毒介导Fg12基因沉默技术对自身免疫性心肌炎大鼠Th1/Th2漂移及Th17/Treg平衡的影响。方法将6周龄SD雄性大鼠随机分为4组,即对照组(NC组)、模型组(Model组)、空载慢病毒组(Vehicle组)、Fgl2-RNAi慢病毒组(RNAi组),每组10只... 目的探讨慢病毒介导Fg12基因沉默技术对自身免疫性心肌炎大鼠Th1/Th2漂移及Th17/Treg平衡的影响。方法将6周龄SD雄性大鼠随机分为4组,即对照组(NC组)、模型组(Model组)、空载慢病毒组(Vehicle组)、Fgl2-RNAi慢病毒组(RNAi组),每组10只。通过注射猪心肌球蛋白建立自身免疫性心肌炎大鼠模型,然后对大鼠尾静脉注射Fgl2-RNAi慢病毒进行免疫。分别在免疫28 d后检测各组大鼠VEDs、LVEDd、LVEF和FS,应用HE染色观察大鼠心肌组织病理情况,通过qRT-PCR和Western blot检测大鼠心肌组织中的IFN-γ、IL-4、IL-17和TGF-βmRNA和蛋白表达。结果建模28 d后,RNAi组的LVEDs和LVEDd显著低于Model组,而RNAi组的LVEF和FS显著高于Model组。Model组、Vehicle组和RNAi组的炎症评分均显著高于NC组,而RNAi组的炎症评分明显低于Model组。RNAi组大鼠心肌组织中的IFN-γ和IL-17 mRNA和蛋白表达水平均显著低于Model组,而IL-4和TGF-βmRNA和蛋白表达水平均显著高于Model组。结论Fg12基因通过调节Th1/Th2漂移及Th17/Treg平衡来参与自身免疫性心肌炎的发生发展,Fg12基因沉默可显著改善自身免疫性心肌炎大鼠的心脏功能,并降低心肌炎症反应。 展开更多
关键词 fg12基因 基因沉默 自身免疫性心肌炎 T细胞亚群 心脏功能 炎症反应
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Expression of Prothrombinase/fibroleukin Gene fg12 in Lung Impairment in a Murine Severe Acute Respiratory Syndrome Model 被引量:1
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作者 Wei-ming YAN  Jia-quan HUANG  +1 位作者 Xiao-ping LUO Qin NING 《中国病毒学》 CSCD 2007年第3期181-192,共12页
To evaluate the role of murine fibrinogen like protein 2 (mfgl2) /fibroleukin in lung impairment in Severe acute respiratory syndrome (SARS), a murine SARS model induced by Murine hepatitis virus strain 3 (MHV-3) thro... To evaluate the role of murine fibrinogen like protein 2 (mfgl2) /fibroleukin in lung impairment in Severe acute respiratory syndrome (SARS), a murine SARS model induced by Murine hepatitis virus strain 3 (MHV-3) through trachea was established. Impressively, all the animals developed interstitial pneumonia with extensive hyaline membranes formation within alveoli, and presence of micro-vascular thrombosis in the pulmonary vessels. MHV-3 nucleocapsid gene transcripts were identified in multiple organs including lungs, spleen etc. As a representative proinflammatory gene, mfgl2 prothrombinase expression was evident in terminal and respiratory bronchioles, alveolar epithelia and infiltrated cells in the lungs associated with fibrin deposition and micro-vascular thrombosis. In summary, the established murine SARS model could mimic the pathologic characteristics of lungs in patients with SARS. Besides the physical damages due to virus replication in organs, the up-regulation of novel gene mfgl2 in lungs may play a vital role in the development of SARS associated lung damage. 展开更多
关键词 凝血酶原酶 fg12基因 肺损伤 急性呼吸综合征 基因表达
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