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目的:观察昆明种H22肝癌小鼠邪毒壅盛证与气虚证肿瘤组织细胞凋亡通路基因表达特征,探讨中医同病异证发生的物质基础。方法:采用小鼠计量化辨证方法,筛选出瘤早期邪毒壅盛证与气虚证同病异证H22肝癌小鼠,采用Affymetrix GeneChip Mouse Exon 1.0 ST Array检测肿瘤组织细胞凋亡通路相关基因表达的特征。结果:依据KEGG数据库细胞凋亡通路,筛选出芯片数据中匹配的33个基因,发现(1)TNF-α和IL-1依赖的细胞凋亡信号通路总体上不利于邪毒壅盛证小鼠肿瘤细胞的凋亡;(2)IL-3依赖的细胞凋亡信号通路总体上反似有利于邪毒壅盛证小鼠肿瘤细胞凋亡;而(3)线粒体介导的细胞凋亡信号通路,邪毒壅盛证小鼠一致表达下调,提示不利于其细胞凋亡。结论:邪毒壅盛肝癌小鼠肿瘤细胞恶性增殖程度高,可能与线粒体介导的细胞凋亡信号通路系列相关基因表达轻度抑制有关。
OBJECTIVE: To observe the gene expression characteristics of apoptotic pathways in Kunming H22 hepatocarcinoma mice and to explore the material basis of TCM syndromes. Methods: We quantified the differentiation of H22 hepatocarcinoma mice with the same pathogenicity by using the quantified syndrome differentiation method of mouse in the early stage of tumorigenesis, using Affymetrix GeneChip Mouse Exon 1.0 ST Array to detect the expression of apoptosis-related genes in tumor tissues feature. Results: According to the apoptotic pathway of KEGG database, we screened out 33 matched genes in the chip data and found that (1) TNF-α and IL-1-dependent apoptotic signaling pathways were not conducive to culturing mice Tumor cell apoptosis; (2) IL-3-dependent apoptotic signaling pathway in general is inversely favored for the apoptosis of tumor cells in culturable mice; and (3) mitochondria-mediated apoptotic signaling pathway , Evil poison 壅 Sheng syndrome mice were down-regulated, suggesting that it is not conducive to its apoptosis. CONCLUSION: The high malignant proliferation of murine hepatocarcinoma cells induced by cultoxin may be related to the mild inhibition of mitochondria-mediated apoptosis-related signal transduction-related gene expression.