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当前位置: 首页 > 文章 > 乳源酪蛋白糖巨肽对NF-κB信号通路中关键蛋白的调控作用 食品科学 2017,38 (17) 26-31
Position: Home > Articles > Regulatory Effect of Milk-Derived Casein Glycomacropeptide on Key Enzymes Involved in NF-κB Signaling Pathway FOOD SCIENCE 2017,38 (17) 26-31

乳源酪蛋白糖巨肽对NF-κB信号通路中关键蛋白的调控作用

作  者：
王泳;龚建苗;贾彦;赵培;庞广昌;阎亚丽;陈庆森
单  位：
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;核因子-κB;磷酸化核因子-κB抑制因子α;泛素-蛋白连接酶亚单位
摘  要：
以结肠癌细胞HT-29为细胞系,在确定乳源性酪蛋白糖巨肽(casein glycomacropeptide,CGMP)对脂多糖(lipopolysaccharides,LPS)诱导的HT-29细胞核因子-κB(nuclear factor-κB,NF-κB)亚单位p65蛋白影响的基础上,在最适作用时间条件下,利用Western blotting技术进一步检测乳源CGMP对NF-κB信号通路上关键蛋白IκBα、p-IκBα、E3RSIκB、UBC5表达水平的影响,以阐述乳源CGMP调控NF-κB信号通路中关键蛋白的作用机制。结果表明:乳源CGMP组的3种质量浓度(0.001、0.010、0.100?μg/m L)均可在一定程度上抑制LPS诱导的HT-29细胞NF-κB信号通路上IκBα蛋白的降解,0.100?μg/m L作用较为明显,与空白对照组比较有显著性差异(P<0.01)。研究明确地证实了乳源CGMP可通过抑制p-IκBα、E3RSIκB、UBC5蛋白的表达来抑制IκBα蛋白的降解,进而抑制NF-κB信号通路的激活。结论:乳源CGMP可显著降低NF-κB信号通路关键蛋白IκBα的降解,其机制是抑制了IκBα的磷酸化和泛素化,使p-IκBα和泛素化关键蛋白E3RSIκB和UBC5的表达均有所下降,进而减少了IκBα的降解,增加了IκBα-p65-p50蛋白三聚体的数量,使p65蛋白核移位效应降低,进而减少下游基因的表达。因此,研究结果科学地阐释了乳源CGMP是通过调控NF-κB信号通路发挥抗炎的作用。
译  名：
Regulatory Effect of Milk-Derived Casein Glycomacropeptide on Key Enzymes Involved in NF-κB Signaling Pathway
作  者：
WANG Yong;GONG Jianmiao;JIA Yan;ZHAO Pei;PANG Guangchang;YAN Yali;CHEN Qingsen;Tianjin Key Laboratory of Food Biotechnology,College of Biotechnology and Food Science,Tianjin University of Commerce;
单  位：
Tianjin Key Laboratory of Food Biotechnology,College of Biotechnology and Food Science,Tianjin University of Commerce
关键词：
casein glycomacropeptide;;colon cancer cells(HT-29);;nuclear factor-κB;;IκBα;;ubiquitin-protein ligase subunit
摘  要：
This study was undertaken to determine the effect of casein glycomacropeptide(CGMP) on the p65 subunit of nuclear factor-κB(NF-κB) of HT-29 human colon cancer cells challenged with lipopolysaccharide(LPS).Furthermore,Western blotting technology was used to detect and compared the expression levels of the key proteins involved in the NF-κB signaling pathway such as IκBα,?p-IκBα,E3RSIκB and UBC5 in the control group,milk-derived CGMP group and LPS group to uncover the molecular mechanism of CGMP in regulating the NF-κB signaling pathway.The results showed that all three doses of CGMP(0.001,0.010 and 0.100 μg/m L) could suppress the degradation of IκBα in some degree,which is involved in the NF-κB signaling pathway of HT-29 cells challenged with LPS and this effect was more significant at the dose of 0.100 μg/m L,which was significantly different when compared with the control group(P < 0.01).Therefore,?it?was?confirmed?that?CGMP?could?suppress?the?degradation?of?IκBα?by?repressing?the?expression?of?p-IκBα,?E3RSIκB?and?UBC5,?thereby?inhibiting?the?activation?of?the?NF-κB?signaling?pathway.?As?a?result,?CGMP?can?significantly?reduce?the?degradation?of?IκBα?in?the?NF-κB?signal?pathway,?increase?the?amount?of?protein?trimer-IκBα-p65-p50? and decrease nuclear translocation of p65 and downstream gene expression by inhibiting the phosphorylation and ubiquitination?of?IκBα?and?reducing?the?expression?of?p-IκBα?and?key?ubiquitin?proteins(E3RSIκB?and?UBC5).?This?study?illustrates?that?milk-derived?CGMP?plays?an?anti-inflammatory?role?by?regulating?the?NF-κB?signal?pathway.

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