Department of Chemistry, Pukyong National University, Busan 48513, Republic of Korea.
Division of Food and Nutrition, Chonnam National University, Gwangju 61186, Republic of Korea.
Food Chem. 2016 Jul 1;202:9-14. doi: 10.1016/j.foodchem.2016.01.114. Epub 2016 Jan 28.
Anti-inflammatory Mytilus edulis hydrolysates (MEHs) were prepared by peptic hydrolysis and MEH was further fractionated into three fractions based on molecular weight, namely >5kDa, 1-5kDa, and <1kDa. The >5kDa peptide fraction exerted the highest nitric oxide (NO) inhibitory activity and inhibited prostaglandin E2 (PGE2) secretion in lipopolysaccharide (LPS)-stimulated RAW264.7 macrophages. Pretreatment with the >5kDa peptide fraction markedly inhibited LPS-stimulated inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) protein and gene expressions. Stimulation by LPS induced the production of pro-inflammatory cytokines, such as tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and -1β (IL-1β), whereas co-treatment with the >5kDa peptide fraction suppressed pro-inflammatory cytokine production. The >5kDa peptide fraction inhibited the translocation of NF-κB (nuclear factor-kappa B) through the prevention of IκBα (inhibitory factor kappa B alpha) phosphorylation and degradation and also inhibited the MAPK signaling pathway in LPS-stimulated RAW264.7 macrophages.
抗炎贻贝水解物（MEHs）通过胃蛋白酶水解制备，然后根据分子量将 MEH 进一步分为三个部分，即>5kDa、1-5kDa 和<1kDa。>5kDa 肽段具有最高的一氧化氮（NO）抑制活性，并抑制脂多糖（LPS）刺激的 RAW264.7 巨噬细胞中前列腺素 E2（PGE2）的分泌。用>5kDa 肽段预处理可显著抑制 LPS 刺激的诱导型一氧化氮合酶（iNOS）和环氧化酶-2（COX-2）蛋白和基因表达。LPS 刺激诱导产生促炎细胞因子，如肿瘤坏死因子-α（TNF-α）、白细胞介素-6（IL-6）和白细胞介素-1β（IL-1β），而用>5kDa 肽段共同处理可抑制促炎细胞因子的产生。>5kDa 肽段通过抑制 IκBα（抑制因子 kappa B alpha）磷酸化和降解来抑制 NF-κB（核因子-kappa B）的易位，并抑制 LPS 刺激的 RAW264.7 巨噬细胞中的 MAPK 信号通路。
