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Casein glycomacropeptide hydrolysates inhibit PGE2 production and COX2 expression in LPS-stimulated RAW 264.7 macrophage cells via Akt mediated NF-κB and MAPK pathways
Food & Function ( IF 5.1 ) Pub Date : 2018-03-27 00:00:00 , DOI: 10.1039/c7fo01989k Tiange Li 1, 2, 3, 4, 5 , Dongxiao Gao 3, 4, 5, 6, 7 , Min Du 8, 9, 10, 11 , Xue Cheng 3, 4, 5, 6, 7 , Xueying Mao 1, 2, 3, 4, 5
Food & Function ( IF 5.1 ) Pub Date : 2018-03-27 00:00:00 , DOI: 10.1039/c7fo01989k Tiange Li 1, 2, 3, 4, 5 , Dongxiao Gao 3, 4, 5, 6, 7 , Min Du 8, 9, 10, 11 , Xue Cheng 3, 4, 5, 6, 7 , Xueying Mao 1, 2, 3, 4, 5
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A casein glycomacropeptide hydrolysate (GMPH) was found to possess inhibitory activity against lipopolysaccharide (LPS)-induced inflammatory response in our previous study. In the current study, the inhibitory effect and the underlying molecular mechanism of GMPH on inflammatory response in LPS-stimulated RAW264.7 macrophages were further investigated. Results showed that GMPH significantly suppressed LPS-induced intracellular reactive oxygen species (ROS) and malondialdehyde (MDA) production. GMPH reduced the production of prostaglandin E2 (PEG2) and the expression of cyclooxygenase-2 (COX-2) and cytosolic phospholipase A2 (cPLA2) in LPS-stimulated macrophages. GMPH also attenuated LPS-induced phosphorylation of MAPK (c-Jun NH2-terminal kinase (JNK), extracellular signal-regulated kinase (ERK) and p38) and protein kinase B (Akt). Furthermore, GMPH inhibited nuclear transcription factor kappa-B (NF-κB) activation by suppressing the nuclear translocation of NF-κB p65, which was markedly reversed by LY294002, an Akt inhibitor. These results demonstrated that GMPH exerts anti-inflammatory functions through the inactivation of MAPK and Akt in LPS-stimulated RAW264.7 macrophages, therefore may hold potential to ameliorate inflammation-related metabolic disorders.
中文翻译：
酪蛋白糖巨肽水解产物通过Akt介导的NF-κB和MAPK途径 抑制LPS刺激的RAW 264.7巨噬细胞中PGE2的产生和COX2的表达
在我们以前的研究中，发现酪蛋白糖巨肽水解产物（GMPH）具有针对脂多糖（LPS）诱导的炎症反应的抑制活性。在当前的研究中，进一步研究了GMPH对LPS刺激的RAW264.7巨噬细胞中炎症反应的抑制作用及其潜在的分子机制。结果表明，GMPH显着抑制LPS诱导的细胞内活性氧（ROS）和丙二醛（MDA）的产生。GMPH减少了LPS刺激的巨噬细胞中前列腺素E2（PEG2）的产生以及环氧合酶2（COX-2）和胞质磷脂酶A2（cPLA2）的表达。GMPH还减弱了LPS诱导的MAPK（c-Jun NH2末端激酶（JNK），细胞外信号调节激酶（ERK）和p38）和蛋白激酶B（Akt）的磷酸化。此外，GMPH通过抑制NF-κBp65的核易位来抑制核转录因子kappa-B（NF-κB）的激活，而AK294抑制剂LY294002可以明显逆转NF-κBp65的核易位。这些结果表明，GMPH通过LPS刺激的RAW264.7巨噬细胞中MAPK和Akt的失活而发挥抗炎功能，因此可能具有缓解炎症相关代谢紊乱的潜力。
更新日期：2018-03-27
中文翻译：
酪蛋白糖巨肽水解产物通过Akt介导的NF-κB和MAPK途径 抑制LPS刺激的RAW 264.7巨噬细胞中PGE2的产生和COX2的表达
在我们以前的研究中，发现酪蛋白糖巨肽水解产物（GMPH）具有针对脂多糖（LPS）诱导的炎症反应的抑制活性。在当前的研究中，进一步研究了GMPH对LPS刺激的RAW264.7巨噬细胞中炎症反应的抑制作用及其潜在的分子机制。结果表明，GMPH显着抑制LPS诱导的细胞内活性氧（ROS）和丙二醛（MDA）的产生。GMPH减少了LPS刺激的巨噬细胞中前列腺素E2（PEG2）的产生以及环氧合酶2（COX-2）和胞质磷脂酶A2（cPLA2）的表达。GMPH还减弱了LPS诱导的MAPK（c-Jun NH2末端激酶（JNK），细胞外信号调节激酶（ERK）和p38）和蛋白激酶B（Akt）的磷酸化。此外，GMPH通过抑制NF-κBp65的核易位来抑制核转录因子kappa-B（NF-κB）的激活，而AK294抑制剂LY294002可以明显逆转NF-κBp65的核易位。这些结果表明，GMPH通过LPS刺激的RAW264.7巨噬细胞中MAPK和Akt的失活而发挥抗炎功能，因此可能具有缓解炎症相关代谢紊乱的潜力。
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