目的:探讨培养液中胆固醇水平对人前列腺癌PC-3细胞生长抑制及凋亡调控的作用。方法:前列腺癌PC-3细胞分别培养于普通和胆固醇缺乏培养液中,再分别加入不同剂量血小板源性生长因子PDGF或EGF作用后,倒置显微镜观察细胞形态,MTT法检测细胞的增殖抑制情况,流式细胞仪进行细胞凋亡率及细胞周期时相分析。结果:与普通培养液组比较,胆固醇缺乏培养液组细胞明显变圆、体积缩小、脱壁细胞增多。MTT法检测显示,胆固醇缺乏培养液组细胞增殖显著抑制,并呈剂量依赖性。流式细胞分析显示胆固醇缺乏培养液组细胞凋亡率同普通培养液组相比无显著差异。当加入PDGF或EGF刺激细胞增殖时,普通培养液组细胞数目显著增加,而在胆固醇缺乏培养液组脱壁细胞增加,细胞凋亡增多,同普通培养液组相比存在显著差异。流式细胞术分析细胞周期显示,同普通培养液组相比,胆固醇缺乏培养液组停滞在G0/G1期细胞增加,而S、G2/M期细胞减少。结论:胆固醇缺乏对PC-3细胞增殖有显著抑制作用,其作用机制并不是简单增加细胞凋亡,而可能是在不利增殖条件下,PC-3细胞的一种自我调节机制。 Objective: To investigate the effects of cholesterol in culture medium on the growth inhibition and apoptosis of human prostate cancer PC-3 cells. Methods: Prostate cancer PC-3 cells were cultured in normal and cholesterol-deficient medium, then treated with different doses of platelet-derived growth factor PDGF or EGF respectively. The morphological changes of the cells were observed under inverted microscope. The proliferation inhibition was detected by MTT assay. Flow cytometry for apoptosis rate and cell cycle phase analysis. Results: Compared with the normal medium group, the cells in the group of cholesterol-deficient medium were significantly rounded, the volume was reduced, and the number of detached cells was increased. MTT assay showed that the cell proliferation was significantly inhibited in a cholesterol-deficient medium and in a dose-dependent manner. Flow cytometry analysis showed that there was no significant difference in apoptosis rate between cholesterol-deficient medium and normal medium. When PDGF or EGF was added to stimulate cell proliferation, the number of cells in the common culture group increased significantly, while in the cholesterol-deficient culture medium group, the number of detached cells increased and the apoptosis increased. Compared with the normal medium group, there was a significant difference. Cell cycle analysis by flow cytometry showed that cells in G0 / G1 phase were arrested in G0 / G1 phase while cells in S, G2 / M phase were decreased compared with those in normal medium. CONCLUSION: Cholesterol deficiency significantly inhibits the proliferation of PC-3 cells. Its mechanism of action is not simply to increase apoptosis, but may be a self-regulatory mechanism of PC-3 cells under unfavorable proliferation conditions.