Preventive effects of marine carotenoids on life-style-related diseases based on anti-inflammatory effects as molecular targets

虾青素对葡聚糖硫酸钠诱导的小鼠结肠炎和炎性相关结肠癌的形成有抑制作用。在给予虾青素的小鼠结肠中，炎性细胞因子α和IL-1β的表达水平通过抑制NF-κB的激活而受到抑制。饲喂20周后，200ppm虾青素饲料可抑制大鼠结肠粘膜溃疡、发育不良隐窝和结肠腺癌的发生。此外，从海洋生物中分离得到的虾青素、果胶烯醇酮、四氧杂黄素和双黄素可减轻内毒素激活的巨噬细胞中炎性细胞因子和COX-2、iNOS的过度表达。饲喂4周后，0.2%岩藻黄质通过抑制α、IL-6等炎性细胞因子的表达，显著抑制胰岛素抵抗大鼠白色脂肪组织中巨噬细胞的表达，从而抑制胰岛素抵抗。此外，岩藻黄质代谢产物岩藻糖醇还通过棕榈酸和肿瘤坏死因子-α调节脂肪细胞和巨噬细胞的串扰。这些结果提示，抗炎作用是岩藻黄质抗肥胖、抗糖尿病作用的分子机制。

Astaxanthin exhibited inhibitory effects on dextran sodium sulfate-induced colitis and inflammatory-related colon carcinogenesis in mice. In colon of the mice fed astaxanthin, mRNA expression levels of inflammatory cytokines such as TNF-α and IL-1β were suppressed through inhibition of NF-κB activation. After feeding for 20 weeks, colonic mucosal ulcers, dysplastic crypts and colonic adenocarcinoma were inhibited by 200 ppm astaxanthin-containing diet. In addition, astaxanthin, pectenolone, alloxanthin and diatoxanthin isolated from marine organisms attenuated excessive mRNA expression of inflammatory cytokines and COX-2 and iNOS in macrophages activated by LPS. On the other hand, dietary 0.2% fucoxanthin markedly suppressed mRNA expression of inflammatory cytokines such as TNF-α and IL-6 to induce insulin resistance and inhibited macrophage infiltration in white adipose tissue through suppression of MCP-1 mRNA expression after 4 weeks feeding. Further, fucoxanthinol, which is one of fucoxanthin metabolites, also regulated cross talk of adipocytes and macrophages via palmitic acid and TNF-α. These results suggest that anti-inflammatory effects are molecular mechanism for anti-obesity and anti-diabetic effects of fucoxanthin.