Grimstad Tore, Bjørndal Bodil, Cacabelos Daniel, Aasprong Ole Gunnar, Janssen Emiel A M, Omdal Roald, Svardal Asbjørn, Hausken Trygve, Bohov Pavol, Portero-Otin Manuel, Pamplona Reinald, Berge Rolf K
Department of Medicine, Division of Gastroenterology, Stavanger University Hospital, Stavanger, Norway.
Scand J Gastroenterol. 2012 Jan;47(1):49-58. doi: 10.3109/00365521.2011.634025. Epub 2011 Nov 30.
To evaluate the effects of krill oil (KO) on inflammation and redox status in dextran sulfate sodium (DSS)-induced colitis in rats.
Thirty male Wistar rats were divided into three groups: Control, DSS, and DSS + KO 5% in a 4-week diet study. Colitis was induced by 5% DSS in the drinking water the last week of the experiment. Weight and disease activity index (DAI), colon length, histological combined score (HCS), colon levels of selected cytokines and prostaglandins, markers of protein oxidative damage, fatty acid profile, and expression of selected genes were measured.
Rats in the DSS group increased their DAI and HCS compared with healthy controls. The colon length was significantly preserved after KO diet. Tumor necrosis factor (TNF)-α and interleukin (IL)-1β were elevated in the DSS group compared with controls. Cytokines and HCS were nonsignificantly lower in the KO versus the DSS group. Prostaglandin (PG)E(3) increased significantly in the KO versus the other groups. Peroxisome proliferator-activated receptor (PPAR)-γ expression was nonsignificantly increased while PPAR-γ coactivator 1α (Pparg1α) expression increased significantly after KO. The levels of protein oxidation markers decreased significantly.
KO showed protective potential against DSS colitis based on the preservation of colon length, reduction of oxidative markers and the consistent beneficial changes of HCS, cytokine, and (PG)E(3) levels, as well as PPAR-γ and Pparg1α expression compared with DSS alone. These findings indicate an anti-inflammatory and a protein antioxidant effect of KO.
评估磷虾油（KO）对葡聚糖硫酸钠（DSS）诱导的大鼠结肠炎炎症和氧化还原状态的影响。
在一项为期4周的饮食研究中，将30只雄性Wistar大鼠分为三组：对照组、DSS组和5% KO + DSS组。在实验的最后一周，通过在饮用水中添加5% DSS诱导结肠炎。测量体重、疾病活动指数（DAI）、结肠长度、组织学综合评分（HCS）、结肠中选定细胞因子和前列腺素的水平、蛋白质氧化损伤标志物、脂肪酸谱以及选定基因的表达。
与健康对照组相比，DSS组大鼠的DAI和HCS升高。KO饮食后结肠长度得到显著保留。与对照组相比，DSS组肿瘤坏死因子（TNF）-α和白细胞介素（IL）-1β升高。与DSS组相比，KO组细胞因子和HCS无显著降低。与其他组相比，KO组前列腺素（PG）E(3)显著增加。过氧化物酶体增殖物激活受体（PPAR）-γ表达无显著增加，而KO后PPAR-γ共激活因子1α（Pparg1α）表达显著增加。蛋白质氧化标志物水平显著降低。
与单独使用DSS相比，基于结肠长度的保留、氧化标志物的减少以及HCS、细胞因子和（PG）E(3)水平以及PPAR-γ和Pparg1α表达的持续有益变化，KO对DSS结肠炎显示出保护潜力。这些发现表明KO具有抗炎和蛋白质抗氧化作用。
