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出 处:《肿瘤研究与临床》2009年第4期226-228,共3页Cancer Research and Clinic
摘 要:目的探讨三萜类化合物熊果酸(UA)诱导卵巢癌细胞SKOV3凋亡的作用。方法用不同浓度的UA处理体外培养的SKOV3细胞,用MTT法、活细胞荧光染色技术、流式细胞术(FCM)、RT—PCR、细胞免疫化学技术,检测UA对SKOV3细胞的增生抑制和诱导凋亡作用。结果UA抑制SKOV3细胞增生,30μmol/L的熊果酸在作用24h后即表现出较强的增生抑制作用,呈时间和浓度依赖性,并使细胞呈典型的凋亡形态学特征,核质浓集,出现凋亡小体,FCM检测显示40μmol/LUA作用24h后SKOV3细胞开始出现G0/G1期阻滞,72h时早期凋亡细胞达(28.7±2.4)%,并诱导野生型p53基因mRNA及蛋白表达增加。结论UA诱导SKOV3细胞凋亡,上调胞内野生型p53基因表达是所涉及的分子机制之一。Objective To study the effect of ursolic acid(UA) on apoptosis of the ovarian cancer cell line SKOV3 and its action mechanisms. Methods The SKOV3 cells were treated with UA at different concentration. The proliferation inhibition was examined by MTT assay. Morphological examination and flow cytometry were used to detect apoptosis. RT-PCR and immunocytochemical method were used to detect the expression of wild type p53,an apoptosis related genes. The semi-quantification of protein expression was analyzed by pathological image-analysis. Results UA inhibited the proliferation of SKOV3 cells strongly. Apoptosis of SKOV3 cells were induced by UA treatment. The morphology of SKOV3 showed changes such as chromatin aggregation, nuclear and cytoplasmic condensation and apoptotic bodies appearance. UA caused significant G0/G1 arrest with a concomitant decrease of cell population in S and G2/M phases. Apoptotic ceils were found by flow cytometry. The maximal early apoptotic rate was (28.7±2.4)% when exposed to 40 μmol/L for 48 h. The expression of p53 gene and protein was enhanced. All these effects were in a dose and time-dependent manner. Conclusion UA induced apoptotic processes in the ovarian cancer SKOV3 cell line were the mechanism involving p53 pathway.
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