白楊素 (Chr) 具有抗發炎及抗氧化特性，並能促進癌細胞死亡。然而，在抑制人類子宮頸癌細胞上的生長及其分子機制並不明瞭。本研究我們檢測 Chr 誘導 HeLa 細胞對 CD95 (APO-1/CD95) 系統、p53、活化 Caspase-3 和粒線體路徑的影響。MTT 試驗，以 Chr 處理會抑制細胞生長及誘導 HeLa 細胞凋亡，使細胞停滯在 G1/G0 期，也增加活性氧自由基 (ROS) 的產生，造成 DNA 斷裂，並促進 Caspase-3 活化及 PARP 分裂，具有劑量及時間依賴效應。Chr 能降低 Bcl-2 及提升 p53 和 Bax 蛋白質的表現。這些結果顯示 Chr 誘導人類子宮頸癌 HeLa 細胞之凋亡的分子機制可能是透過 p53 和粒線體路徑，CD95（APO-1/CD95） 系統及調控 Bcl-2 家族蛋白質所導致。 Chrysin (5, 7-dihydroxyflavone; Chr) possesses potent anti-inflammatory and anti-oxidant properties, and promotes cell death in a number of human cancer cells. However, the intracellular death signaling mechanism(s) by which Chr inhibits human cervix carcinoma cell growth remains poorly understood. In this study, we investigated the effect of CD95 (APO-1/CD95) system, p53, activation of caspase-3 and mitochondrial pathways induced by Chr in human HeLa cells. MTT assay indicated that Chr was cytotoxic in HeLa cells. Chr induced apoptosis, caused cell cycle perturbation (G1/G0-phase arrest), induced the appearance of DNA fragments, promoted cleavage of PARP, and increased the activity of caspase-3 in a dose- and time-dependent manner. While Chr down-regulated the expression of Bcl-2, and up-regulation in p53 and Bax proteins was observed in a dose- and time-dependent pattern. Treatment with Chr for 24 h also induced the generation of ROS with a dose-response effect. Taken together, these results suggest that the mechanism (s) of Chr-triggered apoptosis in HeLa cells could be mediated through the p53 and mitochondrial pathways, CD95 (APO-1/CD95) system and the modulation of Bax, Bcl-2 family proteins.
