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虾青素,一种叶黄素类胡萝卜素,可预防葡聚糖硫酸钠诱导的小鼠结肠炎的发展。

Astaxanthin, a xanthophyll carotenoid, prevents development of dextran sulphate sodium-induced murine colitis.

作者信息

Sakai Shigeki, Nishida Atsushi, Ohno Masashi, Inatomi Osamu, Bamba Shigeki, Sugimoto Mitsushige, Kawahara Masahiro, Andoh Akira

机构信息

Department of Medicine, Shiga University of Medical Science, Seta-Tsukinowa, Otsu 520-2192, Japan.

出版信息

J Clin Biochem Nutr. 2019 Jan;64(1):66-72. doi: 10.3164/jcbn.18-47. Epub 2018 Aug 11.

Abstract

Astaxanthin is a xanthophyll carotenoid, which possesses strong scavenging effect on reactive oxygen species. In this study, we examined the effect of astaxanthin on dextran sulfate sodium (DSS)-induced colitis in mice. Experimental colitis was induced by the oral administration of 4% w/v DSS in tap water in C57BL/6J mice. Astaxanthin was mixed with a normal rodent diet (0.02 or 0.04%). Astaxanthin significantly ameliorated DSS-induced body weight loss and reduced the disease activity index. The ameliorating effects was observed in a dose-dependent manner. Immunochemical analyses showed that astaxanthin markedly suppressed DSS-induced histological inflammatory changes (inflammatory cell infiltration, edematous changes and goblet cell depletion). Plasma levels of malondialdehyde and 8-hydroxy-2-deoxyguanosine were significantly reduced by the administration of 0.04% astaxanthin. Astaxanthin significantly suppressed the mucosal mRNA expression of IL-1β, IL-6, TNF-α, IL-36α and IL-36γ. Astaxanthin blocked the DSS-induced translocation of NF-κB p65 and AP-1 (c-Jun) into the nucleus of mucosal epithelial cells, and also suppressed DSS-induced mucosal activation of MAPKs (ERK1/2, p38 and JNK). In conclusion, astaxanthin prevented the development of DSS-induced colitis via the direct suppression of NF-κB, AP-1 and MAPK activation. These findings suggest that astaxanthin is a novel candidate as a therapeutic option for the treatment of inflammatory bowel disease.

摘要

虾青素是一种叶黄素类胡萝卜素,对活性氧具有很强的清除作用。在本研究中,我们检测了虾青素对葡聚糖硫酸钠(DSS)诱导的小鼠结肠炎的影响。通过给C57BL/6J小鼠口服含4% w/v DSS的自来水诱导实验性结肠炎。将虾青素与正常啮齿动物饮食混合(0.02%或0.04%)。虾青素显著改善了DSS诱导的体重减轻,并降低了疾病活动指数。观察到其改善作用呈剂量依赖性。免疫化学分析表明,虾青素显著抑制了DSS诱导的组织学炎症变化(炎症细胞浸润、水肿变化和杯状细胞减少)。给予0.04%虾青素后,血浆丙二醛和8-羟基-2-脱氧鸟苷水平显著降低。虾青素显著抑制了IL-1β、IL-6、TNF-α、IL-36α和IL-36γ的黏膜mRNA表达。虾青素阻断了DSS诱导的NF-κB p65和AP-1(c-Jun)向黏膜上皮细胞核的转位,还抑制了DSS诱导的黏膜MAPKs(ERK1/2、p38和JNK)的激活。总之,虾青素通过直接抑制NF-κB、AP-1和MAPK激活来预防DSS诱导的结肠炎的发展。这些发现表明,虾青素是治疗炎症性肠病的一种新型治疗选择候选药物。

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