| 摘要: | 1R*, 13S*, 12S*, 9S*, 8R*, 5S*, 4R*)-9-acetoxy-5, 8: 12, 13-diepoxycembr -15(17)-en-16,4-olide是一種Cembranoid類化合物，我們自行命名為ADEO，根據報導指出具有抗癌活性。本研究評估從指形軟珊瑚 Sinularia notanda 分離出的ADEO對人類肝癌 ( Hep G2 ) 細胞的抑制生長活性。結果顯示ADEO具有誘導Hep G2細胞進行細胞凋亡作用。以0~30 μg/ml ADEO來處理Hep G2細胞，發現DNA的斷裂和Sub-G1 peak分佈呈現劑量及時間的效應。ADEO亦能經由誘導Hep G2細胞促使G2/M時期受到停滯而有效地抑制細胞生長。ADEO誘導細胞凋亡能提升調節p53及Bax基因蛋白質的表現，降調節抗細胞凋亡之Bcl-2蛋白質的表現，活化Caspase-3及PARP的裂解。綜合這些研究結果推論出ADEO促使細胞凋亡可能是透過p53相關途徑與調控Bcl-2家族 ( Bax和Bcl-2 )基因蛋白質之表現。
( 1R*, 13S*, 12S*, 9S*, 8R*, 5S*, 4R*)-9-acetoxy-5, 8: 12, 13
-diepoxycembr -15(17)-en-16,4-olide is a cembranoid that has been reported to anticancer activity. We name it of ADEO. In this study, we evaluated the proliferative activity of ADEO isolated from the soft coral of Sinularia notanda in human heptoma ( Hep G2 ) cells. Results demonstrated that ADEO significantly induced human Hep G2 cell undergoing apoptosis. Treatment with 0~30 μg/ml ADEO-triggered cell apoptosis as revealed by the fragmentation of DNA and the subsequent appearance of sub-G1 population in a dose-and time-dependent manner. ADEO also exhibited effective cell growth inhibition by inducing cancer cells to undergo G2/M phase arrest. Data also displayed that ADEO-induced apoptosis involves the up-regulation of p53 and Bax proteins expression, down-regulation of Bcl-2 protein, caspase-3 activation and PARP cleavage. Taken together, these studies suggest that ADEO is an apoptotic inducer that acts on the p53-dependent pathway and modification of Bcl-2 family ( Bax and Bcl-2 ) gene proteins. |
