中文摘要：

目的 了解辣椒素对膀胱癌RT4细胞生长的影响及可能机制.方法 采用细胞计数kit-8（CCK-8）试剂盒观察辣椒素（50、100、150、200、250μmol/L）对膀胱癌RT4细胞生长的影响,以辣椒素（0 μmol/L）为对照组;流式细胞术检测细胞周期和凋亡;逆转录-聚合酶链式反应（RT-PCR）和免疫荧光检测瞬时受体电位香草酸亚型1（TRPV1）的表达;Western印迹检测细胞周期蛋白P53、P21、细胞周期依赖性激酶（CDK）2表达水平.结果 100 μmol/L辣椒素明显抑制RT4细胞生长,细胞成活率为82.0%±6.2%,低于对照组（100.0%±12.4%,P=0.036）,且生长抑制呈剂量依赖性,250μmol/L时细胞成活率仅为7.8%±2.9%（P=0.000）.辣椒素能诱导RT4细胞G0/G1期阻滞,同样呈剂量依赖性,对照组G0/G1期细胞比例为37.4%±5.6%,而250 μmol/L时达到72.4%±5.3%（P=0.000）.RT4细胞表达TRPV1受体mRNA和蛋白.与对照组比较,辣椒素处理后48 h,P53、P21表达上调,而CDK2表达下调.结论 辣椒素可以通过TRPV1受体调节P53、P21、CDK2表达以诱导人膀胱癌RT4细胞G0/G1期阻滞而抑制其生长.

英文摘要：

Objective To study the effects of capsaicin on the growth of bladder cancer RT4 cell and its potential mechanism. Methods Cell counting kit-8 （CCK-8） assay and flow cytometry were employed to observe the effects of capsaicin （50, 100, 150,200, 250 μmol/L） on cell growth, cell cycle and apoptosis. Capsaicin （0μmol/L） was used as a control. The effects of mRNA and protein of transient receptor potential cation channel subfamily V 1 （TRPV1） on RT4 cells were tested by RT-PCR and immunofluoresence respectively. And the expressions of cell cycle protein P53, P21, CDK2 were detected by Western blot after the treatment of capsaicin. Results 100 μmol/L capsaicin significantly decreased the viability of RT4 cell [82.0% ± 6. 2% vs 100. 0% ± 12.4% （ control ）, P = 0. 036] while the cell viability was 7.8% ±2. 9% at 250 μmol/L （P =0. 000）. It was in a dose-dependent manner. On the other hand,capsaicin induced the cell cycle arrest of bladder cancer RT4 cells G0/G1 phase in a dose-dependent way.The cell proportion of G0/G1 phase in the control was 37.4% ±5.6% ,however, it was 72.4% ±5. 3% at 250 μ mol/L （P =0. 000）. It was showed that TRPV1 mRNA and protein were expressed in RT4 cells.After a 48-hour treatment with capsaicin, the expressions of P53 and P21 were up-regulated in contrary to the expression of CDK2. Conclusion Capsaicin induces the cell cycle arrest of bladder cancer RT4 cells G0/G1 phase and growth inhibition via TRPV1 receptor by modulating the expression of P53, P21 and CDK2.