中华肿瘤杂志
中華腫瘤雜誌
중화종류잡지
CHINESE JOURNAL OF ONCOLOGY
2013年
9期
651-654
,共4页
张迎春%杨群培%唐源%王威亚%于建渤%刘卫平
張迎春%楊群培%唐源%王威亞%于建渤%劉衛平
장영춘%양군배%당원%왕위아%우건발%류위평
结外鼻型NK/T细胞淋巴瘤%SNK-6细胞%阿霉素%肿瘤坏死因子相关凋亡诱导配体%细胞凋亡
結外鼻型NK/T細胞淋巴瘤%SNK-6細胞%阿黴素%腫瘤壞死因子相關凋亡誘導配體%細胞凋亡
결외비형NK/T세포림파류%SNK-6세포%아매소%종류배사인자상관조망유도배체%세포조망
Extranodal NK/T-cell lymphoma,nasal type%SNK-6 cell%Doxorubicin%Tumor necrosis factor related apoptosis inducing ligand%Apoptosis
目的 探讨阿霉素对结外鼻型NK/T细胞淋巴瘤SNK-6细胞株肿瘤坏死因子相关凋亡诱导配体(TRAIL)耐受及其受体表达的影响.方法 以不同浓度的阿霉素单独或与TRAIL联合作用于SNK-6细胞,采用四甲基偶氮唑蓝(MTT)法检测细胞的生长情况.采用流式细胞术检测SNK-6细胞的凋亡情况和TRAIL受体的表达情况.结果 100和1000 ng/ml阿霉素单独处理SNK-6细胞24h时,SNK-6细胞的存活率分别为(80.9±7.2)％和(53.7±2.8)％,与联合TRAIL组的差异有统计学意义[分别为(64.9±1.1)％和(34.0±3.9)％,P＜0.05].100和1000 ng/ml阿霉素单独处理SNK-6细胞48 h时,SNK-6细胞的存活率分别为(69.9±6.1)％和(31.1±1.9)％,与联合TRAIL组的差异亦有统计学意义[分别为(37.5±6.4)％和(15.0±1.8)％,P＜0.05].经100和1000 ng/ml阿霉素单独处理48 h后,SNK-6细胞的早期凋亡率分别为(14.8±0.6)％和(30.8±1.5)％,与联合TRAIL组的差异有统计学意义[分别为(28.7±0.6)％和(46.6±2.8)％,P＜0.05].经100 ng/ml阿霉素处理24h后,SHK-6细胞表面TRAIL死亡受体和欺骗受体的表达明显增加.结论 阿霉素在一定程度上可以克服SNK6细胞对TRAIL的耐受,但需要较大剂量的TRAIL才能起作用,这可能与阿霉素同时诱导了TRAIL死亡受体和欺骗受体表达上调有关.
目的 探討阿黴素對結外鼻型NK/T細胞淋巴瘤SNK-6細胞株腫瘤壞死因子相關凋亡誘導配體(TRAIL)耐受及其受體錶達的影響.方法 以不同濃度的阿黴素單獨或與TRAIL聯閤作用于SNK-6細胞,採用四甲基偶氮唑藍(MTT)法檢測細胞的生長情況.採用流式細胞術檢測SNK-6細胞的凋亡情況和TRAIL受體的錶達情況.結果 100和1000 ng/ml阿黴素單獨處理SNK-6細胞24h時,SNK-6細胞的存活率分彆為(80.9±7.2)％和(53.7±2.8)％,與聯閤TRAIL組的差異有統計學意義[分彆為(64.9±1.1)％和(34.0±3.9)％,P＜0.05].100和1000 ng/ml阿黴素單獨處理SNK-6細胞48 h時,SNK-6細胞的存活率分彆為(69.9±6.1)％和(31.1±1.9)％,與聯閤TRAIL組的差異亦有統計學意義[分彆為(37.5±6.4)％和(15.0±1.8)％,P＜0.05].經100和1000 ng/ml阿黴素單獨處理48 h後,SNK-6細胞的早期凋亡率分彆為(14.8±0.6)％和(30.8±1.5)％,與聯閤TRAIL組的差異有統計學意義[分彆為(28.7±0.6)％和(46.6±2.8)％,P＜0.05].經100 ng/ml阿黴素處理24h後,SHK-6細胞錶麵TRAIL死亡受體和欺騙受體的錶達明顯增加.結論 阿黴素在一定程度上可以剋服SNK6細胞對TRAIL的耐受,但需要較大劑量的TRAIL纔能起作用,這可能與阿黴素同時誘導瞭TRAIL死亡受體和欺騙受體錶達上調有關.
목적 탐토아매소대결외비형NK/T세포림파류SNK-6세포주종류배사인자상관조망유도배체(TRAIL)내수급기수체표체적영향.방법 이불동농도적아매소단독혹여TRAIL연합작용우SNK-6세포,채용사갑기우담서람(MTT)법검측세포적생장정황.채용류식세포술검측SNK-6세포적조망정황화TRAIL수체적표체정황.결과 100화1000 ng/ml아매소단독처리SNK-6세포24h시,SNK-6세포적존활솔분별위(80.9±7.2)％화(53.7±2.8)％,여연합TRAIL조적차이유통계학의의[분별위(64.9±1.1)％화(34.0±3.9)％,P＜0.05].100화1000 ng/ml아매소단독처리SNK-6세포48 h시,SNK-6세포적존활솔분별위(69.9±6.1)％화(31.1±1.9)％,여연합TRAIL조적차이역유통계학의의[분별위(37.5±6.4)％화(15.0±1.8)％,P＜0.05].경100화1000 ng/ml아매소단독처리48 h후,SNK-6세포적조기조망솔분별위(14.8±0.6)％화(30.8±1.5)％,여연합TRAIL조적차이유통계학의의[분별위(28.7±0.6)％화(46.6±2.8)％,P＜0.05].경100 ng/ml아매소처리24h후,SHK-6세포표면TRAIL사망수체화기편수체적표체명현증가.결론 아매소재일정정도상가이극복SNK6세포대TRAIL적내수,단수요교대제량적TRAIL재능기작용,저가능여아매소동시유도료TRAIL사망수체화기편수체표체상조유관.
Objective To investigate the effect of doxorubicin on TRAIL resistance and TRAIL receptor expression in lymphoma cell line SNK-6 cells.Methods SNK-6 cells treated with doxorubicin at different concentrations alone or in combination with tumor necrosis factor related apoptosis inducing ligand (TRAIL).Cell proliferation was evaluated by MTT assay.Apoptosis and the expression of TRAIL receptors were determined by flow cytometry.Results MTT assay srhowed that treatment with 100 and 1000 ng/ml doxorubicin for 24 h,the survival rates of SNK-6 cells were (80.9 ± 7.2) ％ and (53.7 ± 2.8) ％,significantly higher than that by treatment combined with 500 ng/ml TRAIL (64.9 ± 1.1) ％ and (34.0 ±3.9)％,respectively (P＜0.05).Flow cytometry showed that after treatment with 100 and 1000 ng/ml doxorubicin for 48 h,the survival rates of SNK-6 cells were (69.9 ± 6.1) ％ and (31.1 ± 1.9) ％,while treated in combination with 500 ng/ml TRAIL,the cell survival rates were (37.5 ± 6.4) ％ and (15.0 ± 1.8) ％,respectively.The early apoptosis rate was (14.8 ± 0.6) ％ and (30.8 ± 1.5) ％,significantly lower than that [(28.7 ±0.6)％ and (46.6 ±2.8)％] after treatment in combination with TRAIL (P ＜0.05).The expressions of TRAIL receptors and decoy receptors were increased when SNK-6 cells were treated with 100 ng/ml doxorubicin for 24 hours.Conclusions Doxorubicin can overcome to a certain extent the TRAIL resistance of SNK-6 cells and induce upregulation of TRAIL death receptors and decoy receptors on the surface of SNK-6 cells.However,a higher dose is needed.
