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作 者:欧阳俊[1] 沈洪[1,2] 刘军楼[1,2] 刘亚军[1,2] 谷静[1]
机构地区:[1]南京中医药大学第一临床医学院,南京210029 [2]江苏省中医院,南京210029
出 处:《世界科学技术-中医药现代化》2014年第4期738-742,共5页Modernization of Traditional Chinese Medicine and Materia Medica-World Science and Technology
基 金:江苏省中医药管理局领军人才培养资助项目(LJ200901):黄芪多糖及β-榄香烯提高消化系肿瘤细胞免疫原性并增强免疫应答的机制研究;负责人:沈洪;江苏省中医院院级课题资助项目(Y11004):通过PI3K/PKB信号传导途径上调自噬活性进而增强肿瘤抗原提呈能力的β-榄香烯抗肝癌免疫机制研究;负责人:沈洪;刘亚军
摘 要:目的:研究中药莪术提取物β-榄香烯对人肝癌HepG2细胞增殖抑制及诱导凋亡,以及小鼠肝癌H22荷瘤小鼠凋亡相关蛋白表达的作用。方法:体外培养人肝癌HepG2细胞,MTT法检测β-榄香烯对细胞增殖的影响,Annexin V-FITC/PI双染检测细胞凋亡。通过建立H22小鼠肝癌荷瘤模型,观察β-榄香烯对荷瘤小鼠肿瘤生长的抑制作用及凋亡相关蛋白的表达。结果:β-榄香烯对HepG2细胞具有抑制增殖的作用,呈剂量和时间的依赖性;Annexin V-FITC/PI法检测到早期凋亡细胞。不同实验组对荷瘤小鼠肿瘤生长的抑制作用程度不同,各药物浓度组Caspase-3蛋白均上调(P<0.05),P65蛋白均下调。结论:β-榄香烯可有效抑制人肝癌HepG2细胞的增殖,其抑制癌细胞增殖的途径是通过诱导细胞发生凋亡,并且与上调凋亡相关蛋白Caspase-3、下调NF-κB P65相关。This article was aimed to study the inhibition of cell proliferation and induction of apoptosis by β-el-emene extract from traditional Chinese medicine (TCM) Rhizoma Zedoariae on human hepatocellular carcinoma (HepG2) cells, as well as the effect on expression of apoptosis-related proteins in liver cancer-burdened H22 mice. Human HepG2 cells were cultured in vitro. MTT method was used in the determination of β-elemene on cell prolif-eration. Apoptosis of cells were detected by the Annexin V-FITC/PI double staining method. Through the establish-ment of liver cancer-burdened H22 mice model, the inhibition of cell proliferation and induction of apoptosis-related protein expression by β-elemene on tumor-burdened mice were observed. The results showed that β-elemene inhib-ited HepG2 cell proliferation, which was dose- and time-dependent. Annexin V-FITC/PI method detected early apoptotic cells. Inhibitions of tumor growth on tumor-burdened mice from different groups were different. Inhibition of tumor growth in the high-dose β-elemene group was relatively low, and that of the middle-dose was more obvi-ous. It was concluded that β-elemene can effectively inhibit human HepG2 cells proliferation. The inhibition on pro-liferation of cancer cells was through the inducing of cell apoptosis. It was also related to the upregulation of apopto-sis-related protein Caspase-3 and downregulation of NF-κB P65.
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