CAJ | 학술논문

目的：探讨蜂毒多肽对人膀胱癌T24细胞的增殖及细胞周期的影响。方法以浓度为0．1、1．0、10．0、100．0μg/ml的蜂毒多肽作用于体外培养的人膀胱癌T24细胞，应用四甲基偶氮唑盐（ MTT）的培养增殖抑制作用，用流式细胞仪检测蜂毒多肽对细胞增殖核抗原（ PCNA）表达及对该细胞周期的影响。结果蜂毒多肽能够在体外抑制人膀胱癌T24细胞的增殖活性；抑制PCNA的表达，呈剂量依赖性，各浓度组PCNA量均较对照组降低（ P ＜0．05或P ＜0．01）；干扰细胞周期，各浓度组G0/G1期均低于对照组（ P ＜0．05或P ＜0．01），S期高于对照组（ P ＜0．05或P ＜0．01），浓度10．0μg/ml和100．0μg/ml组G2/M期均高于对照组（ P ＜0．01）。结论蜂毒多肽可抑制膀胱癌T24细胞的增殖，其作用机制可能与PCNA的表达抑制及细胞周期受到干扰有关。
목적：탐토봉독다태대인방광암T24세포적증식급세포주기적영향。방법이농도위0．1、1．0、10．0、100．0μg/ml적봉독다태작용우체외배양적인방광암T24세포，응용사갑기우담서염（ MTT）적배양증식억제작용，용류식세포의검측봉독다태대세포증식핵항원（ PCNA）표체급대해세포주기적영향。결과봉독다태능구재체외억제인방광암T24세포적증식활성；억제PCNA적표체，정제량의뢰성，각농도조PCNA량균교대조조강저（ P ＜0．05혹P ＜0．01）；간우세포주기，각농도조G0/G1기균저우대조조（ P ＜0．05혹P ＜0．01），S기고우대조조（ P ＜0．05혹P ＜0．01），농도10．0μg/ml화100．0μg/ml조G2/M기균고우대조조（ P ＜0．01）。결론봉독다태가억제방광암T24세포적증식，기작용궤제가능여PCNA적표체억제급세포주기수도간우유관。
Objective To investigate the effect of bee venom peptide on the proliferation and cell cycle of bladder cancer . Methods 0.1,1.0,10.0,100.0 μg/ml concentrations of bee venom peptide were used to act on the cultivated bladder cancers T 24. The propagation supressing measuring method with methyl thiazol tetrazolium (MTT)was applied.Flow cytometry was used to assess the effects of bee venom peptide on the expression of proliferating cell nuclear antigen (PCNA)and cell cycle of T24 bladder cancer cells. Results Bee venom peptide could inhibit proliferation of T 24 bladder cancer cells in vitro and inhibit the expression of proliferating cell nuclear antigen dose-dependently( P <0.05 or P <0.01).Bee venom peptide could interfere with cell cycle of T 24 bladder canc-er cells, decrease G2/M phase cells and increase S phase cells .During interference cell cycle , G0/G1 of each group was lower than that of the control group( P <0.05 or P <0.01),but S phase cells were higher than that of the control group ( P <0.05 or P <0.01), G2M phase of 10μg/ml and 100μg /ml group was higher than that of the control group ( P <0.01).Conlc usoi n Bee venom peptide can inhibite proliferation of T 24 bladder cancer cells .The mechanism may be related to inhibition of PCNA expression and interference with cell cycle .