肿瘤
腫瘤
종류
TUMOR
2010年
3期
175-179
,共5页
高慧洁%张为民%王晓怀%郑锐年
高慧潔%張為民%王曉懷%鄭銳年
고혜길%장위민%왕효부%정예년
乳腺肿瘤%超声疗法%单核细胞%细胞存活%二氢卟吩e6
乳腺腫瘤%超聲療法%單覈細胞%細胞存活%二氫卟吩e6
유선종류%초성요법%단핵세포%세포존활%이경계분e6
Breast neoplasms%Ultrasonic therapy%Monocytes%Cell surcvival%Chlorin-e6
目的:应用二氢卟吩e6作为声敏剂,通过超声波激活,研究其对乳腺癌细胞MDA-MB-231生长的作用. 方法:超声与二氢卟吩e6单独及联合处理MDA-MB-231细胞和正常人外周血单核细胞(peripheral mononuclear cell,PMNC)45 min后,采用MTT比色法检测细胞生长,荧光倒置显微镜下观察细胞形态. 结果:频率1.0 MHz、超声强度1.0～2.0 W/cm~2作用60 s呈强度依赖性抑制PMNC和MDA-MB-231细胞的生长,其抑制50%PMNC和MDA-MB-231细胞生长的超声强度分别为1.23 W/cm~2和1.25 W/cm~2,差异无统计学意义(P>0.05);0.10～1.60 mg/mL二氢卟吩e6呈浓度依赖性地抑制PMNC和MDA-MB-231细胞生长,其抑制PMNC和MDA-MB-231细胞生长的IC_(50)值分别为0.77 mg/mL和0.38 mg/mL, 差异有统计学意义(P<0.05).频率1.0 MHz和超声强度0.5 W/cm~2作用60 s以及0.05～0.20 mg/mL二氢卟吩e6作用两者联合未明显抑制PMNC细胞的生长(P>0.05),但明显抑制MDA-MB-231细胞的生长(P<0.05).细胞形态学观察结果显示,与单纯超声(1.0 MHz频率、0.5 W/cm~2声强作用60 s)及单纯二氢卟吩e6 (0.20 mg/mL) 作用相比,超声联合二氢卟吩e6组的MDA-MB-231细胞死亡率显著增加(P<0.05).结论:超声联合二氢卟吩e6声动力能够特异性抑制乳腺癌MDA-MB-231细胞生长,二氢卟吩e6有望成为一种新型声敏剂应用于乳腺癌的声动力治疗.
目的:應用二氫卟吩e6作為聲敏劑,通過超聲波激活,研究其對乳腺癌細胞MDA-MB-231生長的作用. 方法:超聲與二氫卟吩e6單獨及聯閤處理MDA-MB-231細胞和正常人外週血單覈細胞(peripheral mononuclear cell,PMNC)45 min後,採用MTT比色法檢測細胞生長,熒光倒置顯微鏡下觀察細胞形態. 結果:頻率1.0 MHz、超聲彊度1.0～2.0 W/cm~2作用60 s呈彊度依賴性抑製PMNC和MDA-MB-231細胞的生長,其抑製50%PMNC和MDA-MB-231細胞生長的超聲彊度分彆為1.23 W/cm~2和1.25 W/cm~2,差異無統計學意義(P>0.05);0.10～1.60 mg/mL二氫卟吩e6呈濃度依賴性地抑製PMNC和MDA-MB-231細胞生長,其抑製PMNC和MDA-MB-231細胞生長的IC_(50)值分彆為0.77 mg/mL和0.38 mg/mL, 差異有統計學意義(P<0.05).頻率1.0 MHz和超聲彊度0.5 W/cm~2作用60 s以及0.05～0.20 mg/mL二氫卟吩e6作用兩者聯閤未明顯抑製PMNC細胞的生長(P>0.05),但明顯抑製MDA-MB-231細胞的生長(P<0.05).細胞形態學觀察結果顯示,與單純超聲(1.0 MHz頻率、0.5 W/cm~2聲彊作用60 s)及單純二氫卟吩e6 (0.20 mg/mL) 作用相比,超聲聯閤二氫卟吩e6組的MDA-MB-231細胞死亡率顯著增加(P<0.05).結論:超聲聯閤二氫卟吩e6聲動力能夠特異性抑製乳腺癌MDA-MB-231細胞生長,二氫卟吩e6有望成為一種新型聲敏劑應用于乳腺癌的聲動力治療.
목적:응용이경계분e6작위성민제,통과초성파격활,연구기대유선암세포MDA-MB-231생장적작용. 방법:초성여이경계분e6단독급연합처리MDA-MB-231세포화정상인외주혈단핵세포(peripheral mononuclear cell,PMNC)45 min후,채용MTT비색법검측세포생장,형광도치현미경하관찰세포형태. 결과:빈솔1.0 MHz、초성강도1.0～2.0 W/cm~2작용60 s정강도의뢰성억제PMNC화MDA-MB-231세포적생장,기억제50%PMNC화MDA-MB-231세포생장적초성강도분별위1.23 W/cm~2화1.25 W/cm~2,차이무통계학의의(P>0.05);0.10～1.60 mg/mL이경계분e6정농도의뢰성지억제PMNC화MDA-MB-231세포생장,기억제PMNC화MDA-MB-231세포생장적IC_(50)치분별위0.77 mg/mL화0.38 mg/mL, 차이유통계학의의(P<0.05).빈솔1.0 MHz화초성강도0.5 W/cm~2작용60 s이급0.05～0.20 mg/mL이경계분e6작용량자연합미명현억제PMNC세포적생장(P>0.05),단명현억제MDA-MB-231세포적생장(P<0.05).세포형태학관찰결과현시,여단순초성(1.0 MHz빈솔、0.5 W/cm~2성강작용60 s)급단순이경계분e6 (0.20 mg/mL) 작용상비,초성연합이경계분e6조적MDA-MB-231세포사망솔현저증가(P<0.05).결론:초성연합이경계분e6성동력능구특이성억제유선암MDA-MB-231세포생장,이경계분e6유망성위일충신형성민제응용우유선암적성동력치료.
Objective:To evaluate the sonodynamic effect of chlorin-e6, a sonosensitizing agent, on the proliferation of MDA-MB-231 cells. Methods:MDA-MB-231 and normal peripheral mononuclear cells (PMNCs) were treated with chlorin-e6 alone or combined with ultrasound. Cell proliferation was determined by MTT assay and cell morphology was observed under inversed fluorescence microscope. Results:Treatment with ultrasound (1.0 MHz, 1.0-2.0 W/cm~2,60 s) or chlorin-e6 (0.10-1.60 mg/mL) alone significantly inhibited the cell proliferation of both MDA-MB-231 and PMNC cells in a intensity-dependent and a dose-dependent manner, respectively. The 50% intensity of ultrasound for inhibiting the growth of MDA-MB-231 and PMNC cells was 1.23 W/cm~2 and 1.25 W/cm~2, respectively (P>0.05) and the IC_(50) of chlorin-e6 was 0.38 mg/mL and 0.77 mg/mL, respectively (P<0.05). Compared with single ultrasound (1.0 MHz,0.5 W/cm~2,60 s) or chlorin-e6 (0.05-0.20 mg/mL) treatment, the combination of ultrasound with chlorin-e6 significantly inhibited the proliferation of MDA-MB-231 cells (P<0.05), while had no synergistic inhibitory effects on the growth of PMNC(P>0.05). Compared with single ultrasound treatment (1.0 MHz, 0.5 W/cm~2,60 s) and single chlorin-e6 treatment (0.20 mg/mL), combination of ultrasound and chlorin-e6 significantly increased the death rate of MDA-MB-231 cells (P<0.05). Conclusion:Ultrasound combined with chlorin-e6 exerted specific inhibitory effect on the proliferation of MDA-MB-231 cells. Chlorin-e6 may be a promising sonosensitizing agent for the treatment of breast cancer.
