Kaempferol（3,5,7,4-四氢氟氟烷）的作用，一种类黄酮化合物，在Barnyard Millet（echinochloa crus-gallivar。frumentacea）谷物中被鉴定出来，G2-Checkpoint和poptotic途径在人类的急性clone clone clone clone clone clone clone clone clone clone clone clone clone clone clone clone clone clone clone clone clone clone clone clone clone（或BCl-XL表达矢量（J/BCL-XL）。 J/NEO细胞暴露于Kaempeferol上会导致细胞毒性，ATM/ATR-CHK1/CHK2途径的激活，激活p53（SER-15）的磷酸化，抑制性磷酸化，CDC25C（SER-216）（SER-216）的抑制性磷酸化，以及环蛋白依赖性Kinase 1（CDK1）的灭菌。在这些条件下，凋亡事件包括BAK和PUMA水平上调，BAK激活，线粒体膜电位（ΔPSIM）损失，Caspase-9，-8和-3的激活，抗Poly（ADP-ribose）聚合酶（PARP）聚合酶（PARP）裂解，以及无源性子细胞的积累。 However, these apoptotic events, except for upregulation of Bak and PUMA levels, were completely abrogated in J/Bcl-xL cells overexpressing Bcl-xL, suggesting that the G2-arrest and the Bcl-xL-sensitive mitochondrial apoptotic events were induced, in parallel, as downstream events of the DNA damage-mediated G2-checkpoint activation. Together these results demonstrate that kaempferol-mediated antitumor activity toward Jurkat T cells was attributable to G2-checkpoint activation, which caused not only G2-arrest of the cell cycle but also activating phosphorylation of p53 (Ser-15) and subsequent induction of mitochondria-dependent apoptotic events including Bak and PUMA upregulations, Bak activation, Δpsim loss, and caspase级联激活。