AKTmTORNFκ赏B通路在THP1来源巨噬细胞和梅毒螺旋体感染巨噬细胞极化中的作用研究.docx

优秀毕业论文 精品参考文献资料 摘要酸化程度减弱，炎症因子 摘要 酸化程度减弱，炎症因子IL_lp、TNF．Ⅸ表达受到影响，这与实验前期经典极化 模型的结果基本一致，进一步证明砀通过激活AKT／mTOR／NF—KB通路，引起 巨噬细胞向M1极化。 结论：rp感染巨噬细胞初期，激活了AKT／mTOR／NF—rJ3通路，巨噬细胞向 M1极化，产生大量的炎症因子如IL一1p、TNF．a等，低表达MRC一1，IL—10等抑 制性细胞因子，炎症因子受AKT／mTORfNF．r．B通路抑制剂作用变化，确定了 AKT／mTOR／NF．r,B在梅毒感染巨噬细胞初期对巨噬细胞极化的影响，为进 一步 阐明梅毒的致病机制奠定了一定基础。 关键词：AKT／mTOR／NF．r,B通路；巨噬细胞极化；梅毒螺旋体 万方数据 AbstractAbstract Abstract Abstract Research objects：Syphilis is the sexually transmitted disease caused by Treponema pallidum．The celluar immunity based macrophage take great part in immunity respond to功，macrophage polarization effect syphilis progression AKT／mTOR／NF-r．B pathway occupies important part in regulating the proliferation metabolism and the growth of life movement，it also plays an important part in inflammation，tumor,metabolism．Using AKT／mTOR／NF-r．B pathway the breakthrough point，we can research its regulatory role in macrophage polarization and study the pathogenic mechanism of syphilis from the aspect of macrophage polarization to provide theoretical and experimental basis for treat and prevent syphilis． Methods：In research，we use IFN吖+LPS and IL-4 to construct classical activated macrophages(M 1)and selective activation of macrophages(M2) respectively；then we Western blotting to confirm AKT／mTOR／NF-r33 pathway activation and inhibition situation with inhibitors in different polarization status；then， we infect macrophages with矽，detect the cytokines’expressions 1 2h、24h、48h and 72h by Real Time—PCR to confirm the macrophage polarization status；then，we Western blotting to confirm AKT／mTOR／NF-v．B pathway activation caused by rp； finally,we inhibitors to test their impacts on AKT／mTOR／NF·v,B pathway activation using Western blotting and inflammtory cytokines’expression by Real Time．PCR． Results：THP．1．derived M0 presented with long spindle·shape under the stimulus of lFN吖and LPS，expressed high level IL一1 13、TNF—a、iNOS，expressed low level MRC．1 and on，M0 could be polarized to M 1；THP-1-derived M0 prestented wit