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目的 研究锦鸡丙素对两种人肺癌细胞株中不同组分的蛋白激酶C(PKC)活性及其同工酶分布的影响 ,探讨两种细胞株对锦鸡丙素的细胞生长抑制作用表现出敏感性差异的原因。方法 梯度离心法、32 P掺入法及蛋白印迹法。结果 ①A5 4 9及HCI H4 46细胞所有组分中的PKC活性均可被锦鸡丙素所抑制 ,两种细胞胞质及颗粒组分中PKC活性完全受抑所需时间相同 ,A5 4 9细胞全细胞组分及核组分所需时间均长于NCI H4 46细胞 ;②A5 4 9细胞胞质组分中PKC的活性不可逆转 ,而HCI H4 46细胞为核组分 ;③ 5 4 9细胞中主要表达PKC α、ε和ζ ,胞质中三者都存在 ,颗粒组分中只检测到α且锦鸡丙素处理后α消失 ,而胞质及全细胞组分中的α含量增加 ;NCI H4 46细胞胞质中主要存在PKC ζ和ε,颗粒组分中仅检测到PKC ζ且锦鸡丙素处理后胞质中 ζ增加而颗粒组分中则减少。结论 锦鸡丙素体内外均可抑制PKC的活性并可降低PKC α在颗粒组分中的含量使其膜转位受阻 ,但这种抑制作用与肿瘤细胞生长的抑制之间并没有直接的联系 ;PKC α可能是A5 4 9细胞信号传导系统中最主要的PKC同工酶形式 ,锦鸡丙素抑制其活性并阻碍其膜转位将可能影响A5 4 9肺癌细胞的增殖并与A5 4 9细胞对锦鸡丙素敏感性较高有着密切的关系。
Objective To study the effect of Hesperidin on the protein kinase C (PKC) activity and isoenzyme distribution of two components in human lung cancer cell lines, and to explore the sensitivity of the two cell lines to cell growth inhibition of Hela cells. The reason for sexual differences. Methods Gradient centrifugation, 32 P incorporation and Western blotting. RESULTS: The PKC activity in all components of A549 and HCI H4 46 cells was inhibited by propyltransferase of Jinxi. The time required for the complete inhibition of PKC activity in the cytoplasm and granular components of both cells was the same, and the A5 4 9 cells were all the same. The time required for cell and nuclear components was longer than that of NCI H4 46 cells; the activity of PKC in the cytoplasm fraction of 2A549 cells was irreversible, while the HCI H4 46 cell was the nuclear component; the main expression in 3549 cells was. PKC α, ε, and ζ were all present in the cytoplasm. Only alpha was detected in the particle fraction and α disappeared after treatment with propylpropan in Jinjang, but the α content in cytoplasm and whole cell fractions increased; NCI H4 46 cells PKC ζ and ε were mainly present in the cytoplasm and only PKC ζ was detected in the granule fraction. After treatment with propyl gamma of Jinjang, the amount of quinone in the cytoplasm increased while that in the granule fraction decreased. Conclusion Jinxiong propane inhibited the activity of PKC both in vitro and in vivo and decreased the content of PKC α in the granular fraction, which caused the membrane translocation to be blocked. However, there was no direct relationship between this inhibition and the inhibition of tumor cell growth. PKC α may be the most important form of PKC isoenzyme in the A5 4 9 cell signaling system. Jinxiong C inhibited its activity and impeded its membrane translocation, which may affect the proliferation of A549 lung cancer cells and the A549 cell pairs. The higher sensitivity of the ferriferine propyltransfere has a close relationship.