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[外源性核苷酸对肠上皮细胞增殖和迁移的影响]

[Effects of exogenous nucleotides on the proliferation and migration of intestinal epithelial cells].

作者信息

Chen Xianggui, Wang Ruishu, Deng Maoxian, Ran Xinze

机构信息

Department of Food Engineering, Sichuan University of Science and Technology, Chengdu 610039, China.

出版信息

Wei Sheng Yan Jiu. 2002 Jun;31(3):168-71.

PMID:12545752
Abstract

The effect of exogenous nucleotides on proliferation and migration of a normal rat small intestinal epithelial cell line IEC-6 is studied. The concentration-effects as well as interaction of exogenous nucleotides on proliferation of IEC-6 are measured by MTT. Migration of IEC-6 after wounded is determined by an in vitro model of intestinal epithelial restitution of IEC-6 monolayer. Expression of TGF beta is detected by immunohistochemistry. The results show AMP and GMP remarkably inhibit proliferation of IEC-6 in concentration-dependent manner respectively at 30 mumol/L or 150 mumol/L and more. CMP, UMP and nucleotides mixture can not enhance or inhibit the growth with the exception of inhibition of CMP on proliferation at very high concentration (1440 mumol/L). In contrast, CMP, especially UMP, can remarkably abolish the proliferation-inhibiting effects of AMP or GMP on the cell, when AMP or GMP is supplemented. Nucleotides mixture significantly facilitate migration of IEC-6 after wounded but fail to promote the expression of TGF beta. It is concluded that purine nucleotides inhibits proliferation of IEC-6. Pyrimidine nucleotides can abolish the inhibitive effects of purine nucleotides, and Nucleotides mixture promotes migration of IEC-6 after wounded by a TGF beta-independented way.

摘要

研究外源性核苷酸对正常大鼠小肠上皮细胞系IEC-6增殖和迁移的影响。采用MTT法检测外源性核苷酸对IEC-6增殖的浓度效应及相互作用。通过IEC-6单层肠上皮修复的体外模型测定损伤后IEC-6的迁移。采用免疫组织化学法检测转化生长因子β(TGFβ)的表达。结果显示,AMP和GMP分别在30μmol/L或150μmol/L及以上时,以浓度依赖性方式显著抑制IEC-6的增殖。CMP、UMP和核苷酸混合物除在极高浓度(1440μmol/L)时CMP抑制增殖外,均不能增强或抑制生长。相反,当添加AMP或GMP时,CMP尤其是UMP可显著消除AMP或GMP对细胞的增殖抑制作用。核苷酸混合物显著促进损伤后IEC-6的迁移,但未能促进TGFβ的表达。结论是嘌呤核苷酸抑制IEC-6的增殖。嘧啶核苷酸可消除嘌呤核苷酸的抑制作用,核苷酸混合物通过非TGFβ依赖的方式促进损伤后IEC-6的迁移。

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