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ERK1/2信号途径与弓形虫侵入细胞及胞内增殖关系的研究 被引量:2

Study of the relationship between the ERK1/2 signal pathway and Toxoplasma gondii tachyzoites invading host cells and their proliferation
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摘要 目的探讨阻断细胞外蛋白调节激酶(ERK1/2)信号途径对弓形虫速殖子侵入宿主细胞及在胞内增殖的影响。方法姬氏染色法检测ERK1/2途径不同时间及不同剂量的抑制剂U0126或PD98059作用下宿主细胞感染弓形虫速殖子的百分率,根据细胞感染率和感染细胞内虫荷量分析ERK1/2途径抑制剂对速殖子在细胞中增殖的影响。结果速殖子在细胞培养系统中以1、10和100μmol/L U0126或PD98059作用3 h、6 h和9 h后,前者细胞培养孔中的细胞感染率分别较对照组平均下降34.62%(P<0.01)、53.55%(P<0.01)和67.76%(P<0.01),后者分别较对照组平均下降22.67%(P<0.01)、52.21%(P<0.01)和58.99%(P<0.01);感染细胞感染速殖子率与对照组比较差异无统计学意义(P>0.05)。结论阻断ERK1/2途径的不同信号位点对弓形虫速殖子侵入宿主细胞影响不同,ERK1/2途径在速殖子侵入宿主细胞起主要作用,但对侵入后的增殖无明显影响。 Objective To explore the influence of different inhibitors of extracellular signal-regulated protein kinases(ERK1/2) on Toxoplasma gondii tachyzoites invading host cells and their proliferation in those cells.Methods The inhibitor U0126 or PD98059 was added to a tachyzoite-NIH3T3 cell culture system at different doses,and then the effect on infected cells and the different burden of tachyzoites at different times(3 h-9 h) was analyzed using Giemsa staining.Results The average rate of infection of NIH3T3 cells with 1,10,and 100 μmol/L U0126 decreased to 34.62%,53.55%,and 67.76%,respectively,compared to the control(P0.01).The average rate of infection of NIH3T3 cells with 1,10,and 100 μmol/L PD98059 decreased to 22.67%,52.21% and 58.99%,respectively,compared to the control(P0.01).U0126 or PD98059 had no significant effect on the proliferation of T.gondii tachyzoites in host cells(P0.05).Conclusion ERK1/2 pathway plays an important role in invasion of cells by T.gondii tachyzoites but does not play a role in the regulation of intracellular proliferation.
出处 《中国病原生物学杂志》 CSCD 2011年第3期204-206,212,F0002,共5页 Journal of Pathogen Biology
基金 安徽省高校自然科学研究重点项目(No.KJ2009A046Z) 安徽省教育厅优秀青年科研项目(No.2008jq1140) 蚌埠医学院科研基金项目(No.BY0739)
关键词 刚地弓形虫 速殖子 ERK1/2信号通路 NIH3T3细胞 U0126 PD98059 Toxoplasma gondii tachyzoite extracellular signal-regulated protein kinases(ERK1/2) NIH 3T3 cells U0126 PD98059
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