中外医疗
中外醫療
중외의료
CHINA FOREIGN MEDICAL TREATMENT
2015年
8期
124-126
,共3页
树突状细胞%细胞因子诱导的杀伤细胞%DC-CIK细胞%乳腺癌%免疫治疗
樹突狀細胞%細胞因子誘導的殺傷細胞%DC-CIK細胞%乳腺癌%免疫治療
수돌상세포%세포인자유도적살상세포%DC-CIK세포%유선암%면역치료
Dentritic cell%Cytokine induced killer%Dentritic cell co-cultured cells with cytokine induced killer%Breast Cancer%Immunotherapy
目的:研究DC-CIK细胞和不同浓度顺铂对乳腺癌MCF-7细胞的增殖抑制作用。方法将DC细胞和CIK细胞共同培养得到的DC-CIK细胞与顺铂分别作用于MCF-7细胞,共同培养12h、24 h和48 h,MTT法检测MCF-7细胞的增殖抑制情况,对比DC-CIK细胞和顺铂对MCF-7细胞的增殖抑制效果。结果与DC-CIK细胞共培养12 h、24 h与48 h,MCF-7细胞均出现一定的凋亡,增殖受到明显的抑制;与5×106个DC-CIK细胞共培养12h与40 ng/mL顺铂对其作用12 h的抑制效果相同,共培养24 h与50 ng/mL顺铂对其作用24 h的效果相同,共培养48 h与60 ng/mL顺铂对其作用24 h的效果相同。结论该研究为DC-CIK法治疗乳腺癌作出了实验室基础性研究,为临床DC-CIK细胞抑制乳腺癌细胞提供了理论依据。
目的:研究DC-CIK細胞和不同濃度順鉑對乳腺癌MCF-7細胞的增殖抑製作用。方法將DC細胞和CIK細胞共同培養得到的DC-CIK細胞與順鉑分彆作用于MCF-7細胞,共同培養12h、24 h和48 h,MTT法檢測MCF-7細胞的增殖抑製情況,對比DC-CIK細胞和順鉑對MCF-7細胞的增殖抑製效果。結果與DC-CIK細胞共培養12 h、24 h與48 h,MCF-7細胞均齣現一定的凋亡,增殖受到明顯的抑製;與5×106箇DC-CIK細胞共培養12h與40 ng/mL順鉑對其作用12 h的抑製效果相同,共培養24 h與50 ng/mL順鉑對其作用24 h的效果相同,共培養48 h與60 ng/mL順鉑對其作用24 h的效果相同。結論該研究為DC-CIK法治療乳腺癌作齣瞭實驗室基礎性研究,為臨床DC-CIK細胞抑製乳腺癌細胞提供瞭理論依據。
목적:연구DC-CIK세포화불동농도순박대유선암MCF-7세포적증식억제작용。방법장DC세포화CIK세포공동배양득도적DC-CIK세포여순박분별작용우MCF-7세포,공동배양12h、24 h화48 h,MTT법검측MCF-7세포적증식억제정황,대비DC-CIK세포화순박대MCF-7세포적증식억제효과。결과여DC-CIK세포공배양12 h、24 h여48 h,MCF-7세포균출현일정적조망,증식수도명현적억제;여5×106개DC-CIK세포공배양12h여40 ng/mL순박대기작용12 h적억제효과상동,공배양24 h여50 ng/mL순박대기작용24 h적효과상동,공배양48 h여60 ng/mL순박대기작용24 h적효과상동。결론해연구위DC-CIK법치료유선암작출료실험실기출성연구,위림상DC-CIK세포억제유선암세포제공료이론의거。
Objective To investigate the in-vitro inhibitory efects of DC(dendritic cel1)-CIK (cytokine-induced killer cel1)cocul-tured cells and cis-platinum against breast cancer cell line MCF-7 cells. Methods In this study, the DC cells and CIK cells co-cultured DC-CIK cells and in MCF-7 cells co-cultured for 12, 24 and 48 hours, using the MTT assay MCF-7 cell proliferation inhibition and using different concentrations the chemotherapy drug cisplatin role in MCF-7 cells, using the same MTT assay MCF-7 cell proliferation inhibition. Then compare the inhibitory effect of DC-CIK cells and the chemotherapy drug cisplatin pro-liferation of MCF-7 cells. Results Addition of DC-CIK cells using MTT assay DC-CIK role in the MCF-7 cell proliferation of MCF-7 before and after the show, regardless of the role of 12, 24 or 48 hours, MCF-7 cells apoptosis, proliferation was significant-ly inhibited. DC-CIK and cisplatin on MCF-7 proliferation inhibition comparison, 5 ×106 cells proliferation of MCF-7 cells 12h inhibition with 40 ng/mL concentration of cisplatin on the proliferation of MCF-7 cells for 12h inhibition equivalent for 24h inhib-ited with 50 ng/mL cisplatin equivalent to the inhibition of proliferation of MCF-7 cells 24h, 48h role in the inhibition of 60 ng /ml of cisplatin on the proliferation of MCF-7 cells the 24h of inhibition basic equivalent. The results show that the DC-CIK cells to inhibit the proliferation of MCF-7 cells. Conclusion This study DC-CIK therapy for breast cancer made a laboratory for basic research. In the clinical treatment of breast cancer has a theoretical and experimental basis.