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目的通过诱癌剂N-丁基-N2(4-羟丁基)亚硝胺(BBN)诱发PLC(基因敲除小鼠建立膀胱肿瘤动物模型,为研究PLCε在膀胱肿瘤形成中的作用奠定理论基础。方法随机选取PLC-/-小鼠和PLC+/+小鼠各48只分成A组、B组、C组和D组,A、C为空白对照组饮纯净水,B和D组为实验组饮BBN药水,实验周期为18周,在电子显微镜下观察不同阶段小鼠膀胱肿瘤的发生过程。结果经超微结构证实PLC+/+小鼠发生膀胱肿瘤为15只,占62.5%;PLC-/-小鼠发生膀胱肿瘤为10只,占41.7%。结论成功建立了PLC(基因敲除(PLC-/-)小鼠膀胱肿瘤动物模型,与PLC+/+小鼠相比其膀胱肿瘤的发生率较低,从而验证了PLC(基因与肿瘤发生机制具有相关性,为进一步研究PLC(基因与肿瘤发生机制的关系奠定了基础。
OBJECTIVE: To establish PLC-induced bladder tumor animal model by inducing N-butyl-N2 (4-hydroxybutyl) nitrosamine (BBN) as an inducer of cancer and lay a theoretical foundation for studying the role of PLCε in bladder tumor formation .Methods Forty-eight PLC / / mice and PLC + / + mice were randomly divided into group A, group B, group C and group D. A and C were blank control group drinking purified water, group B and D were experimental Group BBN syrup was used.The experiment period was 18 weeks.Electron microscopy was used to observe the occurrence of bladder tumor in different stages.Results Fifteen bladder tumor was found in PLC + / + mice by ultrastructure, accounting for 62.5% / - The number of bladder tumors in mice was 10, accounting for 41.7% .Conclusion The animal model of bladder cancer in PLC (knockout (PLC - / -) mice was successfully established and the occurrence of bladder tumors compared with PLC + / + mice The lower rate, which verified the PLC (gene and tumor pathogenesis has relevance for further study of PLC (gene and tumor pathogenesis laid the foundation for the relationship.