姜黄素诱导人卵巢癌细胞株A2780凋亡及其分子机制的研究

背景与目的：姜黄素（curcumin）是传统中药姜黄的主要有效成分,其选择性抑制肿瘤细胞增殖并诱导其凋亡作用日益成为研究的焦点,但其中所涉及的机制仍然不十分明确。本研究旨在探讨姜黄素对人卵巢癌细胞株A2780的诱导凋亡效应及其分子机制。方法：10-50μmol/L姜黄素分别处理A2780细胞6-24h后,MTT法检测癌细胞的生长活性;流式细胞仪（FCM）和吖啶橙-溴化乙啶荧光染色法检测细胞凋亡;SP免疫组化法检测细胞内NF-kB蛋白（P65）、caspase-3蛋白表达水平。结果：各浓度姜黄素对癌细胞生长抑制率为62.05％-89.24％,DNA直方图上可见亚“G1“峰;荧光显微镜下部分细胞发生凋亡形态学改变,凋亡率为21.5％-33.5％。NF-kB（P65）表达减弱、caspase-3表达增强,并呈时间依赖性。结论：姜黄素能显著抑制卵巢癌细胞的体外生长;上调caspase-3、下调NF-kB蛋白表达、诱导细胞凋亡可能是其作用机制之一。

Inhibitory effects of curcumin on apoptosis of human ovary cancer cell line A2780 and its molecular mechanism

BACKGROUND & OBJECTIVE: Curcumin is the major effective component of curcuma, which is a kind of traditional Chinese medicine. It has been paid more attention to curcumin recently for its specific proliferation inhibition and apoptosis inducing effects on tumor cells; however, the involved mechanisms were not clear. This study was designed to explore the apoptosis inducing effects of curcumin on human ovary A2780 cell line and its related molecular mechanisms. METHODS: A2780 cancer cells were treated with 10-50 mumol/L curcumin for 6-24 h and the growth inhibition rates of A2780 cancer cells were measured by MTT method. Cell apoptosis was inspected by flow cytometry (FCM) and acridine orange-ethidium bromide fluorescent staining method. The protein levels of NF-kappa B (P65) and Caspase-3 in cancer cells were observed by SP immunohistochemistry. RESULTS: The growth inhibition rates of the cancer cells reached 62.05%-89.24%, with the peak of sub G1 appeared on DNA histogram in FCM. Partial cells presented the characteristic morphological changes of apoptosis under the fluorescent microscope; the apoptosis rates were 21.5%-33.5%. The NF-kappa B (p65) expression was decreased while Caspase-3 expression was increased, which depended on the action time. CONCLUSIONS: Curcumin could significantly inhibit the growth of ovary cancer cells; inducing apoptosis through up-regulating Caspase-3 and down-regulating expression of NF-kappa B was probably one of its molecular mechanisms.