爱普列特对良性前列腺增生体外细胞模型的凋亡诱导作用  被引量:2

Apoptosis induce effect of epristeride on benign prostatic hyperplasia model cells in vitro

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作  者:江振洲[1] 束文慧[1] 张陆勇[1] 严明[1] 孙立[1] 王广基[2] 

机构地区:[1]中国药科大学江苏省新药筛选中心 [2]中国药科大学药物代谢研究中心

出  处:《中国临床药理学与治疗学》2006年第6期644-649,共6页Chinese Journal of Clinical Pharmacology and Therapeutics

基  金:中国药科大学青年教师科技基金项目(№E0223)

摘  要:目的:拟建良性前列腺增生体外细胞模型,并探讨爱普列特(epristeride)对前列腺增生模型中前列腺细胞作用机制。方法:建立大鼠前列腺细胞体外培养方法,给予过量睾酮和多肽生长因子模拟病理环境,探讨诱发前列腺细胞增生的最佳刺激条件,MTT实验观察爱普列特对增生前列腺细胞增殖抑制作用,流式细胞术观察药物对前列腺细胞的凋亡诱导作用。结果:初步建立了良性前列腺增生体外细胞模型,培养液(含睾酮9.08×10-8mol.L-1)培养9 d后,模型组细胞密度显著增高,同时培养液中前列腺特异抗原含量提高。爱普列特作用72 h细胞的IC50值5.0×10-6mol.L-1,流式细胞术分析显示凋亡的特征性亚二倍体峰。结论:雄激素能显著促进体外培养的大鼠前列腺细胞增殖,爱普列特可通过诱导前列腺细胞凋亡发挥对前列腺增生疾病的治疗作用。AIM: To establish a benign prostatic hyperplasia ( BPH ) cells model in vitro and investigate the mechanism of epristeride to BPH cells based on this model. METHODS:Establishing the primary cultural process of rat prostatic cells. In order to stimulate proliferation of the prostatic cells we simulated the pathophysiological environment and added testrone and polypeptide growth factors (PGFs) into the culture medium. MTY reduction assays were used to observe the inhibition effect of epristeride on BPH model cells in vitro, and the apoptosis in-duce effect of epristeride was observed by flow cytometry (FMC). RESULTS: In comparison with normal group, the density of BPH model cells was significantly increased by the stimulation effect of testrone (9.08 × 10^-8 mol·L^-1 ) and PGFs after 9 days; the content of prostate specific antigen in culture medium was increased compared with normal group. The IC50 values of Epriteride to BPH model cells in vitro is 5.0 × 10^-6mol·L^-1 ; The cell apoptosis peak was demonstrated by FMC assay. CONCLUSION: BPH model ceils can be establish in vitro by the stimulation of testrone and PGFs; epristeride can induce apoptosis of BPH model cells in vitro and this mechanism is probably the therapeutical effect in clinical use of epristeride.

关 键 词:良性前列腺增生 多肽生长因子 前列腺特异抗原 5a-还原酶抑制剂 流式细胞术 

分 类 号:R965.1[医药卫生—药理学]

 

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