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Tripeptides from dietary proteins inhibit TNFalpha-induced monocyte adhesion to human aortic endothelial cells.

机译:饮食蛋白中的三肽抑制TNFα诱导的单核细胞粘附于人主动脉内皮细胞。

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Dietary proteins have been shown to reduce atherosclerosis development. Although the components of proteins responsible for this effect are largely unknown, it has been suggested that specific bioactive peptides are involved. In order to elucidate possible atheroprotective mechanisms of bioactive peptides, we evaluated the effect of different tripeptides derived from food proteins on leukocyte-endothelial cell interaction which is regarded as a key event in atherosclerosis development. Treatment of human aortic endothelial cells (HAEC) with 50 microM of Val-Pro-Leu, Ser-Ser-Ser and Glu-Glu-Glu inhibited TNFalpha-induced monocyte adhesion and expression of the adhesion molecule E-selectin (P<0.05). Expression of intercellular adhesion molecule-1 was not influenced by the tripeptides tested in TNFalpha-treated HAEC, whereas expression of vascular cell adhesion molecule-1 was only influenced by Ser-Ser-Ser (P<0.05). Treatment with 50 microM of Ser-Ser-Ser and Glu-Glu-Glu, but not Val-Pro-Leu caused an inhibition of TNFalpha-induced activation of NF-kappaB compared to control cells (P<0.05). In conclusion, the present study shows that short peptides derived from food proteins reduce monocyte adhesion to HAEC. Since monocyte adhesion to the endothelium is a crucial step in the early phase of atherosclerosis, inhibition of monocyte adhesion by bioactive peptides might be one plausible mechanism explaining amelioration of atherosclerotic lesion development by dietary proteins.
机译:饮食中的蛋白质已被证明可以减少动脉粥样硬化的发展。尽管引起这种作用的蛋白质的成分在很大程度上是未知的,但是已经表明涉及特定的生物活性肽。为了阐明生物活性肽的可能的动脉粥样硬化保护机制,我们评估了衍生自食物蛋白的不同三肽对白细胞-内皮细胞相互作用的影响,这被认为是动脉粥样硬化发展的关键事件。用50 microM Val-Pro-Leu,Ser-Ser-Ser和Glu-Glu-Glu处理人主动脉内皮细胞(HAEC)抑制TNFα诱导的单核细胞粘附和粘附分子E-选择素的表达(P <0.05) 。细胞间粘附分子-1的表达不受TNFalpha处理的HAEC中测试的三肽的影响,而血管细胞粘附分子-1的表达仅受Ser-Ser-Ser的影响(P <0.05)。与对照细胞相比,用50 microM Ser-Ser-Ser和Glu-Glu-Glu而不是Val-Pro-Leu进行处理可抑制TNFalpha诱导的NF-κB活化(P <0.05)。总之,本研究表明,源自食物蛋白的短肽减少了单核细胞对HAEC的粘附。由于单核细胞粘附于内皮是动脉粥样硬化早期的关键步骤,因此生物活性肽抑制单核细胞粘附可能是解释膳食蛋白改善动脉粥样硬化病变发展的一种可能机制。

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