肿瘤研究与临床
腫瘤研究與臨床
종류연구여림상
CANCER RESEARCH AND CLINIC
2011年
7期
460-462,466
,共4页
韩江涛%易晓琴%符珉%袁琴香%姚榛祥
韓江濤%易曉琴%符珉%袁琴香%姚榛祥
한강도%역효금%부민%원금향%요진상
乳腺肿瘤%超声疗法%钙%细胞凋亡
乳腺腫瘤%超聲療法%鈣%細胞凋亡
유선종류%초성요법%개%세포조망
Breast neoplasms%Ultrasound therapy%Calcium%Cell apoptosis
目的 探讨高强度超声(HIU)对人类乳腺癌细胞内游离钙浓度的影响及对细胞生长的抑制作用.方法 用HIU(50 W/cm2)干预体外培养的人类乳腺癌细胞MCF-7及MDA-MB-231.用钙离子(Ca2+)荧光探针检测干预后细胞内Ca2+浓度,四甲基偶氮唑蓝(MTT)法榆测干预后细胞生长抑制率,流式细胞术分析细胞周期分布及凋亡率.结果 HIU干预10、20、30 s后,细胞内Ca2+浓度随干预时间的增加而升高,MCF-7细胞分别为(572±20.1)、(670±18.9)、(815±16.3)nmol/L(F=663.65,P＜0.001),MDA-MB-231细胞分别为(582±16.3)、(687±19.7)、(843±14.8)nmol/L(F:863.06,P＜0.001);周期向G0～G1分布,二种细胞G0～G1比例为分别为(60.5±5.5)%、(66.3±7.0)%、(74.5±8.2)%(F=8.17,P=0.002)和(58.5±6.3)%、(66.1±6.3)%、(71.2±7.9)%(F=7.51,P=0.003);凋亡率逐渐上升,二种细胞凋亡率分别为(7.3±1.7)%、(13.2±3.5)%、(19.3±3.7)%(F=18.73,P＜0.001)和(6.3±1.8)%、(11.4±2.3)%、(16.4±3.3)%(F=19.26,P＜0.001);干预后细胞生长抑制率明显增加,二种细胞生长抑制率分别为(9.2±2.2)%、(24.3±3.9)%、(48.6±5.5)%(F=117.16,P＜0.001)和(9.0±1.7)%、(22.3±3.5)%、(41.6±6.4)%(F=71.25,P＜0.001).结论 HIU干预在一定作用时间内使细胞内Ca2+浓度升高,促使细胞周期向G0～G1转化,凋亡率及细胞死亡率明显上升.
目的 探討高彊度超聲(HIU)對人類乳腺癌細胞內遊離鈣濃度的影響及對細胞生長的抑製作用.方法 用HIU(50 W/cm2)榦預體外培養的人類乳腺癌細胞MCF-7及MDA-MB-231.用鈣離子(Ca2+)熒光探針檢測榦預後細胞內Ca2+濃度,四甲基偶氮唑藍(MTT)法榆測榦預後細胞生長抑製率,流式細胞術分析細胞週期分佈及凋亡率.結果 HIU榦預10、20、30 s後,細胞內Ca2+濃度隨榦預時間的增加而升高,MCF-7細胞分彆為(572±20.1)、(670±18.9)、(815±16.3)nmol/L(F=663.65,P＜0.001),MDA-MB-231細胞分彆為(582±16.3)、(687±19.7)、(843±14.8)nmol/L(F:863.06,P＜0.001);週期嚮G0～G1分佈,二種細胞G0～G1比例為分彆為(60.5±5.5)%、(66.3±7.0)%、(74.5±8.2)%(F=8.17,P=0.002)和(58.5±6.3)%、(66.1±6.3)%、(71.2±7.9)%(F=7.51,P=0.003);凋亡率逐漸上升,二種細胞凋亡率分彆為(7.3±1.7)%、(13.2±3.5)%、(19.3±3.7)%(F=18.73,P＜0.001)和(6.3±1.8)%、(11.4±2.3)%、(16.4±3.3)%(F=19.26,P＜0.001);榦預後細胞生長抑製率明顯增加,二種細胞生長抑製率分彆為(9.2±2.2)%、(24.3±3.9)%、(48.6±5.5)%(F=117.16,P＜0.001)和(9.0±1.7)%、(22.3±3.5)%、(41.6±6.4)%(F=71.25,P＜0.001).結論 HIU榦預在一定作用時間內使細胞內Ca2+濃度升高,促使細胞週期嚮G0～G1轉化,凋亡率及細胞死亡率明顯上升.
목적 탐토고강도초성(HIU)대인류유선암세포내유리개농도적영향급대세포생장적억제작용.방법 용HIU(50 W/cm2)간예체외배양적인류유선암세포MCF-7급MDA-MB-231.용개리자(Ca2+)형광탐침검측간예후세포내Ca2+농도,사갑기우담서람(MTT)법유측간예후세포생장억제솔,류식세포술분석세포주기분포급조망솔.결과 HIU간예10、20、30 s후,세포내Ca2+농도수간예시간적증가이승고,MCF-7세포분별위(572±20.1)、(670±18.9)、(815±16.3)nmol/L(F=663.65,P＜0.001),MDA-MB-231세포분별위(582±16.3)、(687±19.7)、(843±14.8)nmol/L(F:863.06,P＜0.001);주기향G0～G1분포,이충세포G0～G1비례위분별위(60.5±5.5)%、(66.3±7.0)%、(74.5±8.2)%(F=8.17,P=0.002)화(58.5±6.3)%、(66.1±6.3)%、(71.2±7.9)%(F=7.51,P=0.003);조망솔축점상승,이충세포조망솔분별위(7.3±1.7)%、(13.2±3.5)%、(19.3±3.7)%(F=18.73,P＜0.001)화(6.3±1.8)%、(11.4±2.3)%、(16.4±3.3)%(F=19.26,P＜0.001);간예후세포생장억제솔명현증가,이충세포생장억제솔분별위(9.2±2.2)%、(24.3±3.9)%、(48.6±5.5)%(F=117.16,P＜0.001)화(9.0±1.7)%、(22.3±3.5)%、(41.6±6.4)%(F=71.25,P＜0.001).결론 HIU간예재일정작용시간내사세포내Ca2+농도승고,촉사세포주기향G0～G1전화,조망솔급세포사망솔명현상승.
Objective Study on the intracellular calcium and growth suppression of human breast cancer cells exposed by high intensity ultrasound (HIU). Methods Exposed human breast cancer cells MDA-MB-231 and MCF-7 in vitro with HIU (50 W/cm2). Examined the intracellular calcium from exposed cells with Fura-2 fluorescence probe. The cell viabilities were measured by MTT assay. The rate of cell apoptosis and distribution of cell cycle were detected on flow cytometry. Results The lever of intracellular calcium went up in pace with exposed time of HIU, MCF-7 cells were (572±20.1), (670±18.9), (815± 16.3) nmol/L (F = 663.65, P＜0.001), MDA-MB-231 cell was (582±16.3), (687±19.7), (843± 14.8) nmol/L (F = 863.06, P＜0.001), and the distribution of cell cycle waved to G0-G1, the ratios of G0-G1 in MCF-7 and MDA-MB-231 were (60.5±5.5)%, (66.3±7.0)%, (74.5±8.2)% (F=8.17, P = 0.002) and (58.5± 6.3) %, (66.1±6.3)%, (71.2±7.9) % (F=7.51, F= 0.003). Apoptotic rate upgraded gradually, the apoptotic rates of MCF-7 and MDA-MB-231 were (7.3±1.7)%, (13.2±3.5) %, (19.3±3.7)% (F= 18.73, P＜0.001) and (6.3±1.8)%, (11.4±2.31)%, (16.4±3.3)% (F = 19.26, P＜0.001). Under MTT assay, the rate of cell growth suppression increased significantly, the rates of cell growth suppression in MCF-7 and MDA-MB-231 were (9.2±2.2) %, (24.3±3.9)%, (48.6±5.5)%(F=117.16, P ＜0.001) and (9.0±1.7)%, (22.3±3.5) %, (416± 6.4)% (F =71.25, P＜0.001). Conclusion HIU enhanced the intracellular calcium of human breast cancer cells within given time and promoted the distribution of cell cycle to G0-G1. The rate of cell apoptosis and the cell's death rate increased evidently.
