姜黄素与LY294002联合应用对前列腺癌PC-3细胞体外生长的影响

【摘要】 目的〓探讨姜黄素与PI3K/Akt抑制剂LY294002联合应用对前列腺癌PC-3细胞体外生长的影响。方法〓根据给药不同将实验分为对照组、姜黄素组、LY294002组和姜黄素组+LY294002联合组,分别加入等量的培养基、25 μmoL/L姜黄素、25 μmoL/L的LY294002和两种混合液。采用MTS法检测各组细胞的增殖情况、流式细胞仪术检测各组细胞凋亡情况、q-PCR测定各组细胞中NF-κB、P53及caspase-9的表达情况。结果〓姜黄素组、LY组和联合组的细胞增值率均较对照组明显降低,且联合组明显低于两个单独用药组(P<0.05)。姜黄素与LY294002联合作用前列腺癌PC-3细胞后,细胞总凋亡率较姜黄素及LY294002单独使用后明显增加(P值均<0.05)。联合用药组的NF-κB表达量明显低于两单独用药组(P<0.05),而P53和caspase-9的表达量均明显高于两单独用药组(P<0.05)。结论〓姜黄素与LY294002联合使用较两种药物单独使用更能有效抑制前列腺癌PC-3细胞的体外生长,作用机制可能是通过抑制NF-κB的表达从而抑制细胞增殖,并增加P53和caspase-9的表达从而促进细胞凋亡来实现的。

Effect of Curcum in combined with LY294002 on cell proliferation of Prostate Carcinoma PC-3 cells

Objective To explore the effect of curcumin in combined with LY294002 on prostate carcinoma PC-3 cells and the possible mechanism. Methods The experiments were divided into four groups according to different drug administration： control group （PPS）, curcumin group （25 μmoL/L of curcumin）, LY group （25 μmoL/L of LY294002） and combination group （mixture of curcumin and LY294002）. Then proliferation viability of PC-3 cells was observed by MTS assay, apoptotic rate was detected by flow cytometry, the mRNA expression of NF-κB,P53 and caspase-9 were examined by Q-PCR, respectively. Results PC-3 cell proliferation was inhibited in three groups, curcumin group, LY294002 group and combination group. The proliferation rate in combination group was more decreased than that in other two groups. The apoptosis rate of PC-3 cells in combination group was significantly increased when compared with curcumin group or LY294002 group （P〈0.05）. NF-κB expression in combination group was also significant lower than curcumin group or LY294002 group （P〈0.05）, while the expression of P53 and caspase-9 in combination group were obviously higher than these in groups of drug administrated alone （P〈0.05）. Conclusion The combined use of curcumin and LY294002 can effectively inhibit the growth of PC-3 cells in vitro, its mechanism might be inhibiting cell proliferation by decreasing the expression of NF-κB, and promoting cell apoptosis by increasing the expression of P53 and caspase-9.