摘要 目的：研究乙酰紫草素(ASK)对人前列腺癌PC-3细胞的诱导凋亡作用及相关的分子机制。方法：利用CCK-8实验检测ASK对体外培养PC-3细胞的杀伤作用;利用流式细胞术实验检测ASK处理后PC-3细胞凋亡情况;利用Western blotting检测凋亡蛋白和AKT信号通路蛋白的表达。结果：CCK-8实验证明ASK能够以时间和浓度依赖性抑制前列腺癌PC-3细胞的增殖;流式细胞术实验证明ASK能够诱导人前列腺癌PC-3细胞线粒体依赖性凋亡;Western blotting证明ASK能够有效抑制前列腺癌PC-3细胞中的AKT信号通路。结论：ASK能够有效抑制人前列腺癌PC-3细胞增殖，并能够有效诱导PC-3细胞发生线粒体依赖性凋亡，其机制可能是通过调控PI3K/Akt信号通路来实现，说明ASK具有一定的抗前列腺癌的潜力。

    关键词 乙酰紫草素;人前列腺癌;PC-3细胞;AKT信号通路;药物诱导;细胞凋亡;分子机制;研究

    Abstract Objective：To study the apoptosis-inducing effects of Acetylshikonin(ASK)on human carcinoma of prostate PC-3 cells and its related molecular mechanisms.Methods：CCK-8 assay was used to detect the killing effects of ASK on PC-3 cells in vitro.Flow cytometry was used to detect the apoptosis of PC-3 cells after ASK treatment.Western blotting was used to detect the expression of apoptotic proteins and AKT signaling pathway proteins.Results：CCK-8 assay demonstrated that ASK can inhibit the proliferation of prostate cancer PC-3 cells in a time and concentration-dependent manner; Flow cytometry experiments showed that ASK can induce mitochondria-dependent apoptosis in carcinoma of prostate PC-3 cells; Western blotting proved that ASK can be effective to inhibit AKT signaling pathway in prostate cancer PC-3 cells.Conclusion：ASK can effectively inhibit the proliferation of human carcinoma of prostate PC-3 cells and can effectively induce mitochondria-dependent apoptosis in PC-3 cells.The mechanism may be achieved by regulating PI3K/Akt signaling pathway ......