甲硫基蛋氨酸通过JAK2-STAT5-NF-κB和MAPK信号通路在牛乳腺上皮细胞中发挥抗炎作用,Journal of Agricultural and Food Chemistry

当前位置： X-MOL 学术 › J. Agric. Food Chem. › 论文详情

Our official English website, www.x-mol.net, welcomes your feedback! (Note: you will need to create a separate account there.)

甲硫基蛋氨酸通过JAK2-STAT5-NF-κB和MAPK信号通路在牛乳腺上皮细胞中发挥抗炎作用
Journal of Agricultural and Food Chemistry ( IF 5.7 ) Pub Date : 2020-11-12 , DOI: 10.1021/acs.jafc.0c05962
Wei Lan ₁ , Zhen Wang ₁ , Jianxin Liu ₁ , Hongyun Liu ₁

Affiliation

甲硫基蛋氨酸（Met-Met）是一种功能性二肽。尽管二肽在乳蛋白合成中的作用已明确确立，但Met-Met是否在牛乳腺上皮细胞（MAC-T）炎症中具有抗炎作用和保护机制仍然未知。这项研究的目的是确定Met-Met对脂多糖（LPS）诱导的MAC-T细胞炎症的有益作用及其潜在机制。进行RNA-seq，siRNA干扰和western印迹以确定在LPS暴露情况下Met-Met的抗炎机制。用2 mM Met-Met预处理可以减少TNF-α（3.14±0.55 vs 1.54±0.26，P <0.01），IL- 1β（2.30±0.21 vs 1.86±0.11，PLPS暴露后<0.05）和IL-8（3.49±0.29 vs 0.62±0.20，P <0.01）。RNA-seq分析表明，重叠的基因主要富集于核因子κB（NF-κB），促分裂原活化蛋白激酶（MAPK）和IL-17途径。Met-Met对NF-κB，P38和JNK的抑制作用是通过Janus激酶2信号转导子和转录激活因子5（JAK2-STAT5）途径介导的。此外，通过敲低JAK2逆转了Met-Met介导的LPS诱导的p-IκB，NF-κB和JNK激活的减少。总体而言，Met-Met通过激活JAK2-STAT5途径，然后抑制NF-κB和MAPK信号传导途径，对MAC-T细胞炎症产生有益作用。

"点击查看英文标题和摘要"

Methionyl-Methionine Exerts Anti-Inflammatory Effects through the JAK2-STAT5-NF-κB and MAPK Signaling Pathways in Bovine Mammary Epithelial Cells

Methionyl-methionine (Met-Met) is a functional dipeptide. Although the role of a dipeptide in milk protein synthesis is clearly established, whether Met-Met has an anti-inflammatory effect and a protective mechanism in bovine mammary epithelial cell (MAC-T) inflammation remains unknown. The purpose of this study was to determine the beneficial effects and underlying mechanisms of Met-Met on lipopolysaccharide (LPS)-induced MAC-T cell inflammation. RNA-seq, siRNA interference, and western blotting were performed to determine the anti-inflammatory mechanisms of Met-Met in the context of LPS exposure. Pretreatment with 2 mM Met-Met could reduce the increase in TNF-α (3.14 ± 0.55 vs 1.54 ± 0.26, P < 0.01), IL-1β (2.30 ± 0.21 vs 1.86 ± 0.11, P < 0.05), and IL-8 (3.49 ± 0.29 vs 0.62 ± 0.20, P < 0.01) after 1 μg/mL LPS exposure. RNA-seq analyses indicated that the overlapping genes were primarily enriched in the nuclear factor kappa-B (NF-κB), mitogen-activated protein kinase (MAPK), and IL-17 pathways. The suppression of NF-κB, P38, and JNK by Met-Met was mediated through the Janus kinase 2-signal transducers and activators of transcription 5 (JAK2-STAT5) pathway. Moreover, the Met-Met-mediated decrease in the LPS-induced activation of p-IκB, NF-κB, and JNK was reversed by knocking down JAK2. Collectively, Met-Met has beneficial effects on MAC-T cell inflammation by activating the JAK2-STAT5 pathway and then inhibiting the NF-κB and MAPK signaling pathways.

更新日期：2020-11-25

点击分享查看原文

点击收藏

阅读更多本刊新发论文本刊介绍/投稿指南