中国肿瘤生物治疗杂志
中國腫瘤生物治療雜誌
중국종류생물치료잡지
CHINESE JOURNAL OF CANCER BIOTHERAPY
2010年
1期
46-50
,共5页
李卿%王新利%王杨%隋承光
李卿%王新利%王楊%隋承光
리경%왕신리%왕양%수승광
肝肿瘤%树突状细胞%细胞因子活化的杀伤细胞%索拉菲尼
肝腫瘤%樹突狀細胞%細胞因子活化的殺傷細胞%索拉菲尼
간종류%수돌상세포%세포인자활화적살상세포%색랍비니
hepatocarcinoma%dendritic cell%cytokine-induced killer cell%sorafenib
目的:观察DC、CIK共培养细胞(DC-CIK)联合索拉菲尼(sorafenib)对肝癌细胞BEL-7402的体内外杀伤效应.方法:取健康人外周血单个核细胞,加入不同细胞因子促进DC及CIK细胞成熟并混合共培养.CCK8试剂盒检测DC-CIK共培养细胞联合索拉菲尼对BEL-7402细胞的体外杀伤效应,Annexin V-FITC试剂盒检测两者联合对肝癌细胞凋亡率的影响.用肝癌细胞BEL-7402建立裸鼠皮下移植瘤模型,分为生理盐水对照组、索拉菲尼组、DC-CIK组、DC-CIK+索拉菲尼组,观察它们对裸鼠移植瘤生长的抑制作用.结果:联合组对肝癌细胞的杀伤率及诱导凋亡率均明显高于各单独治疗组,联合组杀伤率高达(75.24±1.91)%,是DC-CIK组的1.8倍,是索拉菲尼单药组的2.1倍(P<0.01);联合组诱导肝癌细胞凋亡率达(78.32±2.54)%,与单独治疗组相比差异有统计学意义(P<0.05).体内实验表明,DC-CIK+索拉菲尼组可明显抑制裸鼠BEL-7402移植瘤的生长,抑制率为(83.37±0.16)%,与单独治疗组相比差异有显著统计学意义(P<0.01).结论:DC-CIK共培养细胞联合索拉菲尼在体内、外可显著抑制肝癌细胞的生长,分子靶向治疗联合细胞免疫治疗可能成为肝癌综合治疗的方法之一.
目的:觀察DC、CIK共培養細胞(DC-CIK)聯閤索拉菲尼(sorafenib)對肝癌細胞BEL-7402的體內外殺傷效應.方法:取健康人外週血單箇覈細胞,加入不同細胞因子促進DC及CIK細胞成熟併混閤共培養.CCK8試劑盒檢測DC-CIK共培養細胞聯閤索拉菲尼對BEL-7402細胞的體外殺傷效應,Annexin V-FITC試劑盒檢測兩者聯閤對肝癌細胞凋亡率的影響.用肝癌細胞BEL-7402建立裸鼠皮下移植瘤模型,分為生理鹽水對照組、索拉菲尼組、DC-CIK組、DC-CIK+索拉菲尼組,觀察它們對裸鼠移植瘤生長的抑製作用.結果:聯閤組對肝癌細胞的殺傷率及誘導凋亡率均明顯高于各單獨治療組,聯閤組殺傷率高達(75.24±1.91)%,是DC-CIK組的1.8倍,是索拉菲尼單藥組的2.1倍(P<0.01);聯閤組誘導肝癌細胞凋亡率達(78.32±2.54)%,與單獨治療組相比差異有統計學意義(P<0.05).體內實驗錶明,DC-CIK+索拉菲尼組可明顯抑製裸鼠BEL-7402移植瘤的生長,抑製率為(83.37±0.16)%,與單獨治療組相比差異有顯著統計學意義(P<0.01).結論:DC-CIK共培養細胞聯閤索拉菲尼在體內、外可顯著抑製肝癌細胞的生長,分子靶嚮治療聯閤細胞免疫治療可能成為肝癌綜閤治療的方法之一.
목적:관찰DC、CIK공배양세포(DC-CIK)연합색랍비니(sorafenib)대간암세포BEL-7402적체내외살상효응.방법:취건강인외주혈단개핵세포,가입불동세포인자촉진DC급CIK세포성숙병혼합공배양.CCK8시제합검측DC-CIK공배양세포연합색랍비니대BEL-7402세포적체외살상효응,Annexin V-FITC시제합검측량자연합대간암세포조망솔적영향.용간암세포BEL-7402건립라서피하이식류모형,분위생리염수대조조、색랍비니조、DC-CIK조、DC-CIK+색랍비니조,관찰타문대라서이식류생장적억제작용.결과:연합조대간암세포적살상솔급유도조망솔균명현고우각단독치료조,연합조살상솔고체(75.24±1.91)%,시DC-CIK조적1.8배,시색랍비니단약조적2.1배(P<0.01);연합조유도간암세포조망솔체(78.32±2.54)%,여단독치료조상비차이유통계학의의(P<0.05).체내실험표명,DC-CIK+색랍비니조가명현억제라서BEL-7402이식류적생장,억제솔위(83.37±0.16)%,여단독치료조상비차이유현저통계학의의(P<0.01).결론:DC-CIK공배양세포연합색랍비니재체내、외가현저억제간암세포적생장,분자파향치료연합세포면역치료가능성위간암종합치료적방법지일.
Objective: To investigate the in vitro and in vivo inhibitory effects of DC (dendritic cell)-CIK (cytokine-induced killer cell) co-cultured cells combined with sorafenib against hepatocellular carcinoma cell line BEL-7402. Methods: DC and CIK cells were generated in vitro by stimulating human peripheral blood mononuclear cells with different cytokines, and then they were co-cultured. The cytotoxicity of DC-CIK co-cultured cells (DC-CIK) combined with sorafenib against BEL-7402 cells was determined by CCK8 kit. The apoptosis of BEL-7402 cells was measured by Annexin V-FITC Kit. BEL-7402-implanted tumor model was established by subcutaneous injection in nude mouse. Tumor-bearing mice were divided into normal saline control group, sorafenib group, DC-CIK group and DC-CIK+sorafenib group. The inhibitory effects were observed in different groups. Results: The cytotoxicity rate of BEL-7402 cells in DC-CIK+sorafenib group was significantly higher than those in the other two groups, with cytotoxicity rate in DC-CIK+sorafenib group being (75.24±1.91)%, which was 1.8 times that in DC-CIK group and 2.1 times that in sorafenib group (P<0.01). The apoptosis rate of BEL-7402 cells in DC-CIK+sorafenib group was significantly higher than those in the sorafenib and DC-CIK groups, with the apoptosis rate in DC-CIK+sorafenib group being (78.32±2.54)% (P<0.05). The volume of tumor in the combination group was significantly smaller than those in the other groups (P<0.05). In vivo results showed that DC-CIK+sorafenib treatment significantly inhibited the growth of BEL-7402-implanted tumors, and the inhibitory rate was (83.37 ±0.16)%, which was significantly higher than those of the other groups (P<0.01). Conclusion:DC-CIK co-cultured cells combined with sorafenib can inhibit the growth of hepatocellular carcinoma cell line BEL-7402 in vitro and in vivo. Molecular targeting therapy combined with immunotherapy may be a new way for the comprehensive treatment of hepatocellular carcinoma.