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当前位置: 首页 > 文章 > 乳源酪蛋白糖巨肽作用人结肠癌细胞HT-29调控炎症活力研究 食品科学 2017 (15) 201-207
Position: Home > Articles > Milk-Derived Casein Glycomacropeptide(CGMP) Regulates Inflammation in Human Colon Carcinoma Cells HT-29 FOOD SCIENCE 2017 (15) 201-207

乳源酪蛋白糖巨肽作用人结肠癌细胞HT-29调控炎症活力研究

作  者：
王泳;龚建苗;贾彦;阎亚丽;庞广昌;赵培;陈庆森
单  位：
天津商业大学生物技术与食品科学学院天津市食品生物技术重点实验室
关键词：
酪蛋白糖巨肽;结肠癌细胞HT-29;NF-κB信号途径;NF-κB必需调节蛋白;细胞凋亡
摘  要：
为进一步阐释乳源酪蛋白糖巨肽(casein glycomacropeptide,CGMP)的抗炎及修复肠道炎症的功效,本研究在确定了乳源CGMP对脂多糖(lipopolysaccharides,LPS)诱导的结肠癌细胞HT-29NF-κB亚单位p65蛋白的影响和乳源CGMP调控核转录因子(nuclear factor,NF)-κB信号通路的基础上,通过构建表达乳源CGMP和NF-κB必需调节蛋白(NF-κB essential modulator,NEMO)的质粒,共转HT-29细胞,免疫共沉淀测定两个蛋白的相互作用。最后采用线粒体膜电位法测定乳源CGMP对HT-29细胞的促凋亡作用。结果表明,乳源CGMP与NEMO(NF-κB essential modulator)30 h共转HT-29细胞中,乳源CGMP与NEMO蛋白均表达,且表现出二者的相互作用。乳源CGMP可与NEMO相互作用影响NF-κB信号通路;同时乳源CGMP还促进HT-29细胞凋亡,呈时间依赖性,其中0.1μg/m L的CGMP作用效果最好。乳源CGMP与NEMO相互作用是间接作用于IκB激酶(IκB kinase,IKK)而作用于?IκB,进而影响NF-κB信号通路。研究揭示了乳源CGMP调控NF-κB信号通路的另一种途径,也充分说明乳源CGMP可通过作用多种抗炎途径发挥其调控作用。
译  名：
Milk-Derived Casein Glycomacropeptide(CGMP) Regulates Inflammation in Human Colon Carcinoma Cells HT-29
作  者：
WANG Yong;GONG Jianmiao;JIA Yan;YAN Yali;PANG Guangchang;ZHAO Pei;CHEN Qingsen;Tianjin Key Laboratory of Food Biotechnology,College of Biotechnology and Food Science,Tianjin University of Commerce;
关键词：
casein glycomacropeptide(CGMP);;colon carcinoma cells HT-29;;NF-κB signaling pathway;;NF-κB essential modulator(NEMO);;apoptosis
摘  要：
To further elucidate the anti-inflammatory activity of casein glycomacropeptide(CGMP) and its efficacy in enhancing recovery from intestinal inflammation, the effect of CGMP on the NF-κB p65 subunit in colon carcinoma cells HT-29 treated with lipopolysaccharide(LPS) and its role in regulating the NF-κB signaling pathway were determined. Furthermore, plasmids were constructed to express CGMP and NF-κB essential modulator(NEMO) and then used to co-transfect HT-29 cells. Co-immunoprecipitation was used to identify the interaction between the expressed proteins. Finally, we detected the pro-apoptotic effect of CGMP on HT-29 cells by measuring the change in mitochondrial transmembrane potential. The experimental results indicated that after 30 h transfection of HT-29 cells, the co-expression and interaction of CGMP and NEMO were confirmed. CGMP affected the NF-κB signaling pathway through its interaction with NEMO with a concomitant increase in apoptosis of HT-29 cells in a time-dependent manner. This effect of CGMP was maximum at 0.1 μg/m L. In conclusion, the interaction of CGMP and NEMO can indirectly affect IKK(IκB kinase) and therefore the NF-κB signaling pathway through IκB. The study revealed another way CGMP could regulate the NF-κB signaling pathway, and fully indicated that there are multiple ways CGMP could execute anti-inflammatory effect.

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