%0 Journal Article
%T 酸性环境抑制CIK细胞对肝癌HepG2细胞的杀伤活性
%A 丁妍
%A 于莉
%A 李东升
%A 王小莉
%A 郭兴荣
%A 袁雅红
%J 肿瘤防治研究
%D 2016
%R 10.3971/j.issn.1000-8578.2016.05.003
%X 摘要 目的 研究酸性环境对CIK（cytokine-induced killer, CIK）细胞杀伤肝癌HepG2细胞的影响。方法 利用IFN-γ、IL-2及CD3抗体诱导外周血单个核细胞获得CIK细胞。在pH6.5及pH7.4条件下将CIK细胞和荧光素酶标记的HepG2细胞（HepG2-luc）按不同的效靶比混合培养，用小动物活体成像系统检测HepG2-luc荧光强度并计算杀伤活性，用MTT法检测并计算杀伤活性。在pH6.5及pH7.4条件下，在含CIK条件培养液0、50%和100%的情况下培养HepG2细胞，流式细胞仪检测凋亡坏死的细胞比例。结果 pH7.4时CIK细胞对HepG2细胞的杀伤率明显高于pH6.5时。CIK条件培养液作用下，pH7.4时HepG2细胞的凋亡坏死比例明显高于pH6.5。结论 酸性环境明显抑制了CIK细胞对肝癌细胞HepG2的杀伤活性
%K CIK
%K 酸性环境
%K HepG2
%K 杀伤活性
%K Effects of GSTP1 on Proliferation and Invasion of Human HepG2 Cells
%K Effects of Silencing B7-H3 Gene on Invasion of Human Hepatocellular Carcinoma Cells
%K Betanin Induces Nuclear Necrosis and Mitochondria Intact of HeLa
%K HepG2 and A549 Cells
%K Establishment of Hepatocellular Carcinoma Cell Line HepG2 Stably Transfected by Hepatitis B Virus X Gene and Its Effects on p53-p21 Pathway
%K Screening of Effective STAT5A siRNAs and Their Influence on Proliferation and#br# Apoptosis in Human Hepatocellular Carcinoma Cell Line HepG2
%K Effects of SEPT9 Gene Silencing on Cell Proliferation and Apoptosis of HepG2 Hepatoma Cells
%K Expressions of DR5
%K caspase-8
%K caspase-9 and caspase-3 in HepG2 Cell Line Treated with Gemcitabine
%K Effects of Intrathoracic DC-CIK Treatment and Chemotherapy on Immune Indexes in Malignant Pleural Effusion
%K Effects of 5-Aza-2′-deoxycytidine on Apoptosis and Expression of PEG10 Gene in Human Hepato Carcinoma Cell Line HepG2
%K Inhibitory Effects on HepG2 Cells from Genetic Engineering Cells Secreted Tumor Necrosis Factor
%K Effect of CIK Treatment on Localized Renal Carcinoma Patients after Radical Operation
%K Significance of Caspase in NS-398 Induced Apoptosis of HepG2 Cell Line
%K Anti-proliferative Effect of Combining Paeonol and Doxorubicin on HepG2 Cell
%K Anti-proliferation and Inducing Apoptosis Effects of CIK Cells Against Breast Cancer Cell Lines
%K Cloning and Identification of Caspase-3 Gene from HepG2 Cells that Underwent Autophagic Apoptosis
%U http://www.zlfzyj.com/CN/abstract/abstract8741.shtml