Casein Lactose-Glycation of the Maillard-Type Attenuates the Anti-Inflammatory Potential of Casein Hydrolysate to IEC-6 Cells with Lipopolysaccharide Stimulation.
Casein Lactose-Glycation of the Maillard-Type Attenuates the Anti-Inflammatory Potential of Casein Hydrolysate to IEC-6 Cells with Lipopolysaccharide Stimulation.
复制标题
DOI：
10.3390/nu14235067
复制
发表时间：
2022-11-29
期刊：
影响因子：
5.9
通讯作者：
Zhao XH
中科院分区：
文献类型：
--
作者：
Chen N;Fu Y;Wang ZX;Zhao XH
在乳制品的热加工过程中，乳蛋白和乳糖之间发生美拉德反应，形成包括糖化蛋白在内的各种产物。在本研究中，酪蛋白与乳糖通过美拉德反应生成乳糖糖化酪蛋白，然后用胰蛋白酶水解。以脂多糖（LPS）刺激的大鼠肠上皮细胞（IEC-6）为细胞模型，以相应的酪蛋白水解物（CH）为对照，研究了所得糖基化酪蛋白水解物（GCH）的抗炎作用。结果表明，预形成的糖基化使乳糖与酪蛋白结合，使GCH的乳糖含量为12.61 g/kg蛋白，但其活性低于CH，从而提高了IEC-6细胞的活力值。LPS刺激后的细胞表现出明显的炎症反应，而在LPS刺激前对细胞进行预处理的GCH持续导致三种促炎介质IL-6、IL-1β和肿瘤坏死因子-α (TNF-α)的分泌减少，但两种抗炎介质IL-10和转化生长因子-β (TGF-β)的分泌增加，表明GCH在LPS刺激的细胞中具有抗炎潜力。此外，GCH上调受刺激细胞中TLR4、p-p38和p-p65蛋白的表达，导致NF-κB和MAPK信号通路受到抑制。总的来说，GCH在细胞中发挥这些被评估的抗炎活性的效率大多低于CH，更重要的是，GCH还显示出通过促进IL-6分泌和上调TLR4和p-p65表达而引起细胞炎症的能力。因此，maillard型酪蛋白乳糖糖基化可以减弱酪蛋白水解产物的抗炎作用。值得注意的是，maillard型酪蛋白乳糖糖基化可能会对酪蛋白在肠道内的生物活性产生负面影响，因为消化后糖基化的酪蛋白会释放GCH，其抗炎活性降低。
During the thermal processing of dairy products, the Maillard reaction occurs between milk proteins and lactose, resulting in the formation of various products including glycated proteins. In this study, lactose-glycated casein was generated through the Maillard reaction between casein and lactose and then hydrolyzed by a trypsin preparation. The anti-inflammatory effect of the resultant glycated casein hydrolysate (GCH) was investigated using the lipopolysaccharide (LPS)-sitmulated rat intestinal epithelial (IEC-6) cells as a cell model and corresponding casein hydrolysate (CH) as a control. The results indicated that the preformed glycation enabled lactose conjugation to casein, which endowed GCH with a lactose content of 12.61 g/kg protein together with a lower activity than CH to enhance the viability value of the IEC-6 cells. The cells with LPS stimulation showed significant inflammatory responses, while a pre-treatment of the cells with GCH before LPS stimulation consistently led to a decreased secretion of three pro-inflammatory mediators, namely, IL-6, IL-1β and tumor necrosis factor-α (TNF-α) but an increased secretion of two anti-inflammatory mediators, including IL-10 and transforming growth factor-β (TGF-β), demonstrating the anti-inflammatory potential of GCH in LPS-stimulated cells. In addition, GCH up-regulated the expression of TLR4, p-p38, and p-p65 proteins in the stimulated cells, resulting in the suppression of NF-κB and MAPK signaling pathways. Collectively, GCH was mostly less efficient than CH to exert these assessed anti-inflammatory activities in the cells and more importantly, GCH also showed an ability to cause cell inflammation by promoting IL-6 secretion and up-regulating the expression of TLR4 and p-p65. The casein lactose-glycation of the Maillard-type was thereby concluded to attenuate the anti-inflammatory potential of the resultant casein hydrolysate. It is highlighted that the casein lactose-glycation of the Maillard-type might cause a negative impact on the bioactivity of casein in the intestine, because the glycated casein after digestion could release GCH with reduced anti-inflammatory activity.
登录
查看更多内容
影响因子：
8.8
作者：
Gu, Feng-Lin;Kim, Jin Moon;Chen, Zheng-Xing
通讯作者：
Chen, Zheng-Xing
影响因子：
6
作者：
Mengibar, Marian;Miralles, Beatriz;Heras, Angeles
通讯作者：
Heras, Angeles
影响因子：
5.2
作者：
Figueroa-Lozano, Susana;Valk-Weeber, Rivca L.;de Vos, Paul
通讯作者：
de Vos, Paul
影响因子：
5.9
作者：
Chen N;Wang L;Zhang Q;Zhao XH;Shi J
通讯作者：
Shi J
影响因子：
6.1
作者：
Jiang, Fan;Guan, Haining;Han, Jianchun
通讯作者：
Han, Jianchun