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作 者:白文坤[1,2] 杨少玲[1] 申锷[1] 王玉[1] 胡兵[1]
机构地区:[1]上海交通大学附属第六人民医院超声医学科上海超声医学研究所,200233 [2]山东省千佛山医院超声诊疗科,济南250014
出 处:《中华超声影像学杂志》2012年第10期902-905,共4页Chinese Journal of Ultrasonography
基 金:上海市科委基础研究重点项目(10JC1412600)
摘 要:目的研究低频低能量超声联合微泡诱导人雄激素非依赖型前列腺癌细胞凋亡及可能分子机制。方法以频率21kHz、声强为46mW/cm2超声,采用连续波,辐照人前列腺癌PC-3细胞悬液。实验分3组:对照组、单纯超声组和超声联合微泡组(加声诺维200μ1)。辐照后,细胞集落实验检测对细胞增殖的影响;辐照后培养24h,透射电镜及TUNEL染色检测细胞凋亡,实时定量PCR检测对Bcl-2/BaxtuRNA表达的影响。结果超声联合微泡组细胞集落数量明显少于对照组(153.33±10.80对313.33±25.82,P〈0.05),超声联合微泡能明显抑制人前列腺癌细胞的增殖。超声联合微泡组较对照组能明显诱导细胞凋亡(13.33±1.35对0.33±0.17,P〈0.05)。超声联合微泡能够下调Bcl-2tuRNA的表达,上调BaxtuRNA的表达(P〈0.05)。结论低频低能量超声联合微泡能够诱导人雄激素非依赖型前列腺癌细胞凋亡,并且可能通过下调Bcl-2rrlRNA及上调BaxmRNA的表达来实现。Objective To study whether low-frequency and low-energy ultrasound combined with microbubbles induced apoptotic cell death in androgen-independent prostate cancer cells and to identify the probable mechanism. Methods Ultrasound with a frequency of 21 kHz and intensity of 46 mW/cm2 in continuous wave mode was used. PC-3 cells were divided three groups:control group,ultrasound group and ultrasound combined with microbubbles. Ultrasound combined with microbubbles group was added 200 μ1 SonoVue. After treatment, colony assay was used to study cell proliferation. Twenty-four hours after treatment,transmission electron microscopy and TUNEL were used to measure cell apoptosis. Real-time PCR was used to measure the expression of the apoptosis-related mRNA, Bcl^2 and Bax. Results Ultrasound combined with microbubbles group's colony number was significantly less than the control group's colony number (153.33 ± 10.80 vs 313.33 ± 25.82, P 〈 0.05). Ultrasound combined with microbubbles group induced more apoptosis in PC-3 cells than did the control group (13.33 ± 1.35 vs 0.33 ± 0.17, P 〈0.05). Treatment with ultrasound combined with microbubbles decreased the expression of Bel-2,an anti-apoptotic mRNA,and increased the expression of Bax, a pro-apoptotic mRNA. Conclusions Ultrasound combined with microbubbles induced apoptotic cell death in human prostate cancer PC-3 cells through down-regulation of Bcl-2 and up-regulation of Bax.
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