低氧状态下PI3K/Akt通路调控髓核细胞存活的实验研究

目的 探讨低氧对体外培养的髓核细胞存活的影响及PI3K/Akt通路在其中可能的作用.方法 体外培养大鼠髓核细胞,以去铁敏(DFX)干预模拟低氧状态,采用MTT比色法检测细胞存活的变化,Western blot检测Akt及磷酸化Akt的表达变化.以PI3K抑制剂LY294002作用于髓核细胞,检测上述指标的变化情况.结果 低氧状态下髓核细胞存活比例较正常氧分压状态下有增加,二者差异有统计学意义,此过程中Akt及磷酸化Akt的表达均上调.PI3K抑制剂LY294002处理可部分逆转该现象.结论 低氧可以促进髓核细胞存活,PI3K/Akt通路部分参与对该过程的调控.

Hypoxic regulation of nucleus pulposus cells survival via PI3K/Akt pathway

Objective To investigate the effect ofhypoxia on survival ofmonolayer cultured nucleus pulposus cells and the possible role of PI3K/Akt pathway in this process. Methods Rat nucleus pulposus cells were excluded, digested and monolayer cultured in vitro. Hypoxic conditions were mimicked by treatment with a chemical compound desferrioxamine （DFX）. Cell survival was measured with MTT assay and the protein expression of Akt and phospho-Akt was detected by Western blot. Moreover, changes of cell survival and Akt expresision were detected by PI3K inhibitor LY294002. Results Compared with normoxic condition, nucleus pulposus cell sruvival increased under hypoxic condition, which had a statistical difference between this two condition. During this process, the Akt and phospho- Akt expressions were upregulated. Treatment with LY294002 resulted in downregulation of cell survival. Conclusions Hypoxia contributes to the cell survival of nucleus pulposus. PI3K/Akt pathway regulates cell survival in nucleus pulposus under hypoxia.