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sIL-13Rα2 抑制IL-13介导的NIH-3T3胶原I的合成及血吸虫病肝组织中sIL-13Rα

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sIL-13Rα2 抑制IL-13介导的NIH-3T3胶原I的合成及

血吸虫病肝组织中sIL-13Rα2/IL-13的表达

李静;王维;李小月;储德勇;闻慧琴;周银娣;张诗海;罗庆礼;沈继龙

【期刊名称】《中国人兽共患病学报》 【年(卷),期】2009(025)008

【摘要】To determine the inhibition of IL-13 by recombinant sIL-13Rα2 in NIH-3T3 fibroblast cells for its potential therapeutic value in hepatic fibrosis caused by Schistosoma japanicum in mice . IL-13 and sIL-13Rα2 from liver of BALB/c mice infected with S.japonicum at different infection time (weeks 0,6,8,10 and 12) were analyzed by ELISA and RT-PCR. The recombinant sIL-13Rα2 expression plasmidwas constructed, followed by transfection into NIH-3T3 fibroblast cells. TypeⅠcollagen produced by NIH-3T3 cells were examined by RT-PCR and Western blotting. It was demonstrated that the expression of IL-13 increased gradually after infection, reached peak density (16.1586 pg/mL)at week 8 and then reduced but was still higher than the level of control mice(3.4146 pg/mL;P =0.017 ). The secretion of sIL-13R α2 reached to its peak 10 weeks after infection(4827.426 pg/mL)and then reduced slowly but still higher than normal(4057.112 pg/mL; P=0.021). Meanwhile, the changes in mRNA level of IL-13 and sIL-13R α2 were coincided with that examined by ELISA. Both IL-13 and sIL-13Rα2 reached their peak density (P=0.033) at week 8 and 10 (P=0.025)

sIL-13Rα2 抑制IL-13介导的NIH-3T3胶原I的合成及血吸虫病肝组织中sIL-13Rα

sIL-13Rα2抑制IL-13介导的NIH-3T3胶原I的合成及血吸虫病肝组织中sIL-13Rα2/IL-13的表达李静;王维;李小月;储德勇;闻慧琴;周银娣;张诗海;罗庆礼;沈继龙【期刊名称】《中国人兽共患病学报》【年(卷),期】2009(025)008【摘要】Todeterminetheinhibit
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