Rice protein hydrolysates (RPHs) inhibit the LPS-stimulated inflammatory response and phagocytosis in RAW264.7 macrophages by regulating the NF-κB signaling pathway

被引:28
|
作者
Wen, Li [1 ,2 ]
Chen, Yuehua [1 ]
Zhang, Li [2 ]
Yu, Huixin [2 ]
Xu, Zhou [1 ]
You, Haixi [1 ]
Cheng, Yunhui [1 ]
机构
[1] Changsha Univ Sci & Technol, Dept Food & Biol Engn, Coll Chem & Biol Engn, 960,2nd Sect,Wangjiali South Rd, Changsha 410114, Hunan, Peoples R China
[2] Jiangsu Inst Nucl Med, Key Lab Nucl Med, Jiangsu Key Lab Mol Nucl Med, Minist Hlth, Wuxi 214063, Jiangsu, Peoples R China
来源
RSC ADVANCES | 2016年 / 6卷 / 75期
基金
中国国家自然科学基金;
关键词
NITRIC-OXIDE SYNTHASE; TOLL-LIKE RECEPTORS; BIOACTIVE PEPTIDES; CYTOKINE PRODUCTION; INNATE; EXPRESSION; CELLS; PURIFICATION; IDENTIFICATION; ACTIVATION;
D O I
10.1039/c6ra08927e
中图分类号
O6 [化学];
学科分类号
0703 ;
摘要
The antioxidant and anti-hypertension properties of rice peptides following hydrolysis by proteolytic enzymes have been investigated previously, but the anti-inflammatory and immune characteristics have not been fully explored. In this study, we investigated the inhibitory effects of trypsin-derived rice protein hydrolysates (RPHs) on the inflammatory response in LPS-stimulated RAW264.7 macrophages, and probed their underlying molecular mechanisms of action. Moreover, a fraction, RPHs-C-7-3, displayed significant inflammation suppression activity by inhibiting the release of nitric oxide (NO) and tumour necrosis factor-alpha (TNF-alpha). Transcription of TNF-alpha, inducible nitric oxide synthase (iNOS), interleukin-6 (IL-6), and interleukin-1 beta (IL-1 beta) were decreased in a dose-dependent manner. Additionally, RPHs-C-7-3 attenuated iNOS and repressed the nuclear transcription factor (NF-kappa B) signaling pathway by impeding the nuclear translocation of p65. RPHs-C-7-3 also repressed the phagocytic ability of the activated macrophages. Our results demonstrated that RPHs exerted anti-inflammatory effects in LPS-stimulated RAW264.7 macrophages and may therefore have potential for treating inflammation-related conditions.
引用
收藏
页码:71295 / 71304
页数:10
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