The preventive mechanisms of life-style related disease by edible plant extracts and their application for the disease

本研究的目的如下。一是了解芦荟、绿茶、月见草等提取物的抗肿瘤作用机制。在月见草萃取物对艾氏腹水癌细胞的抗肿瘤作用机制方面，我们证明月见草萃取物(EPP)可诱导艾氏腹水癌细胞(EATC)凋亡并抑制其DNA合成，提示月见草萃取物抑制EATC生长的作用至少有两条途径，分别受活性氧(特别是细胞内过氧化物质)的调节。它们是(A)EPE诱导的依赖于过氧化氢增加的细胞凋亡途径和(B)EPE诱导的不依赖于过氧化氢的细胞增殖抑制。在这项研究中，EPE导致细胞内多胺水平显着下降。此外，多胺的加入逆转了EPE诱导的细胞活力下降，并抑制了EPE诱导的细胞内过氧化氢的增加。然而，多胺的加入并不能逆转EPE引起的DNA合成和Rb蛋白磷酸化的降低，以及EPE引起的AIF移位。这些结果表明，多胺参与了EPE诱导的细胞凋亡途径，该途径依赖于过氧化氢的增加。我们还检测了绿茶提取物和茶多酚对FK-506诱导的肾细胞毒性的保护作用。免疫抑制剂FK506的肾毒性限制了其广泛应用。

The purposes of this study are following. One is to understand the mechanisms of antitumor activity of extracts of Aloe, green tea, evening primrose and others. Another is to examined the effect of combined treatment of these extracts.On the mechanism of antitumor activity of evening primrose extract in Ehrlich ascites tumor cells, we demonstrated that evening primrose extract (EPP) induced apoptosis and inhibited the DNA synthesis in Ehrlich ascites tumor cells (EATC) and suggested that EPE-induced inhibition of the growth of EATC are via at least two pathway differentially modulated by reactive oxygen species, notably intracellular peroxides. These are (a) the EPE-induced apoptosis pathway which is dependent on increases in hydrogen peroxide and (b) the EPE-induced inhibition of cell proliferation which is hydrogen peroxide independent. In this study EPE brought about a significant decrease in intracellular polyamine levels. Furthermore, the addition of polyamines reversed the EPE-induced decrease in cell viability and suppressed the EPE-induced increase in intracellular hydrogen peroxide. However, the addition of polyamines did not reverse EPE-induced decrease in DNA synthesis and phosphorylation of Rb protein, and EPE-induced translocation of AIF. These results suggest the involvement of polyamines in EPE-induced apoptosis pathway which is dependent on increase in hydrogen peroxide. We also examined the protective effect of green tea extract and tea polyphenols against FK-506-induced cytotoxicity in renal cells. The nephrotoxicity induced by the immunosuppressive drug FK506 limits its usefulness in widespread application.