高强度超声对人乳腺癌MCF-7细胞COX-2非依赖性凋亡作用的探讨  

The mechanism of apoptosis in COX-2 independent way from MCF-7 cells by high intensity ultrasound

作　　者：韩江涛[1] 刘振林[1] 鹿文静[1] 易晓琴[1] 符珉[1] 林琦远[2] 

机构地区：[1]宜宾市第一人民医院超声科,四川宜宾644000 [2]成都大学医学院

出　　处：《西部医学》2010年第10期1799-1801,共3页Medical Journal of West China

基　　金：宜宾市重点科技项目(No.200703007)

摘　　要：目的探讨高强度超声对人乳腺癌MCF-7细胞的环氧化酶-2非依赖性凋亡作用。方法用高强度超声(50w/cm2)干预体外培养的人乳腺癌MCF-7细胞。RT-PCR检测干预前后MCF-7的COX-2mRNA的相对水平,透射电镜观察细胞超微结构。MTT检测干预后细胞生长抑制率。结果高强度超声干预前后,COX-2mRNA皆呈阴性表达,随着干预时间的增加,电镜下凋亡小体明显增加。干预时间增加到30秒,细胞出现死亡的形态学改变,MTT可见细胞生长抑制率明显增加。结论高强度超声干预在一定作用时间内促进乳癌MCF-7细胞环氧化酶-2非依赖性的细胞凋亡。Objective To study the mechanism of apoptosis in COX-2 independent way in MCF-7 cells by high intensity ultrasound.Methods Human breast cancer cells MCF-7 were treated in vitro with high intensity ultrasound.The relative levels of COX-2 mRNA were detecdted by RT-PCR assay.The ultrastructural changes in apoptotic cells were confirmed by transmission electron microscopy and the cell viabilities were measured by MTT assay.Results The expression of COX-2 mRNA was negative around the exposure time.Under electron microscope,apoptotic bodies in MCF-7 cells were considerably increased.When time extended to 30 seconds,there were died cells.The rate of cell growth suppression in MCF-7 was increased significantly.Conclusions High intensity ultrasound can promote the apoptosis of breast cancer cells MCF-7 in a COX-2mRNA independent way.

关 键 词：高强度超声 COX-2MRNA 乳腺癌 凋亡 

分 类 号：R73-3[医药卫生—肿瘤]