Yang Ming-gen, Zheng Zhou-da, Lin Hai-li, Zhuang Zhi-ming, Lin Tian-qi
Zhonghua Nan Ke Xue. 2015 Feb;21(2):113-8.
To investigate the effects of simvastatin on the proliferation and apoptosis of prostatic epithelial RWPE-1 cells.
RWPE-1 cells cultured in vitro were treated with simvastatin at 0, 10, 20, and 40 μmol/L for 24, 48, and 72 hours followed by determination of their proliferation by MTT assay, and their apoptosis by flow cytometry. The mRNA and protein expressions of Bcl-2, Bax, and Cx43 were detected by fluorescence quantitative RT-PCR and Western blot, respectively.
After 72 hours of treatment with simvastatin at 10, 20, and 40 μmol/L, the inhibition rates of the RWPE-1 cells were (21.07 ± 6.41)%, (34.87 ± 9.65)%, and (47.18 ± 10.88)%, respectively, significantly higher than (1.21 ± 0.54)% in the control group (P < 0.05) and in a dose-dependent manner (P < 0.05); the cell apoptosis rates were (0.066 ± 0.016)%, (0.126 ± 0.023)%, and (0.192 ± 0.025)%, respectively, remarkably higher than (0.015 ± 0.005)% in the control (P < 0.05) and also in a dose-dependent manner (P < 0.05); the mRNA and protein expressions of Bcl-2 were decreasing while those of Bax and Cx43 increasing with the increased concentration of simvastatin (P < 0.05). The expression of Cx43 was correlated negatively with that of Bcl-2 but positively with that of Bax.
Simvastatin inhibits the proliferation of prostate epithelial cells and induce their apoptosis by acting on the gap junctional intercellular communication.
探讨辛伐他汀对前列腺上皮RWPE - 1细胞增殖和凋亡的影响。
体外培养的RWPE - 1细胞分别用0、10、20和40 μmol/L辛伐他汀处理24、48和72小时,然后通过MTT法测定其增殖情况,通过流式细胞术测定其凋亡情况。分别采用荧光定量RT - PCR和Western blot检测Bcl - 2、Bax和Cx43的mRNA和蛋白表达。
用10、20和40 μmol/L辛伐他汀处理72小时后,RWPE - 1细胞的抑制率分别为(21.07 ± 6.41)%、(34.87 ± 9.65)%和(47.18 ± 10.88)%,显著高于对照组的(1.21 ± 0.54)%(P < 0.05),且呈剂量依赖性(P < 0.05);细胞凋亡率分别为(0.066 ± 0.016)%、(0.126 ± 0.023)%和(0.192 ± 0.025)%,明显高于对照组的(0.015 ± 0.005)%(P < 0.05),也呈剂量依赖性(P < 0.05);随着辛伐他汀浓度增加,Bcl - 2的mRNA和蛋白表达降低,而Bax和Cx43的表达增加(P < 0.05)。Cx43的表达与Bcl - 2呈负相关,与Bax呈正相关。
辛伐他汀通过作用于细胞间缝隙连接通讯抑制前列腺上皮细胞增殖并诱导其凋亡。