蛇床子素诱导人前列腺癌LNCaP细胞凋亡及其分子机制

The molecule mechanisms of cell apoptosis induced by osthole in prostate cancer LNCaP cells

目的探讨天然化合物蛇床子素对人前列腺癌LNCaP细胞凋亡的影响及其分子机制。方法采用CCK8法检测蛇床子素对前列腺癌LNCaP细胞增殖的影响;荧光电子显微镜下观察细胞核形态的变化;流式细胞仪AnnexinV-FITC/PI双染法检测蛇床子素诱导细胞凋亡情况;Western blot法检测凋亡相关蛋白Bax、bcl-2的表达情况。结果蛇床子素对LNCaP细胞增殖有明显的剂量依赖性抑制作用,诱导细胞凋亡,可见典型的细胞凋亡改变,且与凋亡率呈一定剂量相关性。随着蛇床子素浓度的增加,凋亡相关蛋白bcl-2的表达减少、Bax的表达增加。结论蛇床子素诱导前列腺癌LNCaP细胞凋亡,与调节凋亡相关蛋白Bax、bcl-2的表达相关。

Objective To study the molecule mechanisms of prostate cancer LNCaP cells apoptosis induced by osthole. Methods CCK8 assay was used to measure the cell proliferation, apoptosis was investigated by fluorescent electron microscope and flow cytometric analysis using an Annexin V-FITC/PI apoptosis kit. The expressions of Bax and bcl-2 were detected by Western blot. Results The growth of LNCaP cells was suppressed by osthole in a dose-dependent manner, osthole induced LNCaP cells apoptosis in a dose-dependent manner and apoptosis cells were observed by fluorescent electron microscope. Osthole decreased the expression level of apoptosis-related protein bcl-2, but increased Bax expression level in a concentration dependent manner. Conclusion Osthole induce LNCaP cells apoptosis,which is related to regulating the expression of apoptosis-related proteins Bax and bcl-2.