Agista Afifah Zahra, Rusbana Tubagus Bahtiar, Islam Jahidul, Ohsaki Yusuke, Sultana Halima, Hirakawa Ryouta, Watanabe Kouichi, Nochi Tomonori, Budijanto Slamet, Yang Suh-Ching, Koseki Takuya, Aso Hisashi, Komai Michio, Shirakawa Hitoshi
Laboratory of Nutrition, Graduate School of Agricultural Science, Tohoku University, 468-1 Aramaki Aza Aoba, Aoba-ku, Sendai 980-8572, Japan.
Department of Food Technology, Faculty of Agriculture, University of Sultan Ageng Tirtayasa, Serang 42110, Indonesia.
Nutrients. 2021 May 30;13(6):1869. doi: 10.3390/nu13061869.
Fermented rice bran (FRB) is known to protect mice intestines against dextran sodium sulfate (DSS)-induced inflammation; however, the restoration of post-colitis intestinal homeostasis using FRB supplementation is currently undocumented. In this study, we observed the effects of dietary FRB supplementation on intestinal restoration and the development of fibrosis after DSS-induced colitis. DSS (1.5%) was introduced in the drinking water of mice for 5 days. Eight mice were sacrificed immediately after the DSS treatment ended. The remaining mice were divided into three groups, comprising the following diets: control, 10% rice bran (RB), and 10% FRB-supplemented. Diet treatment was continued for 2 weeks, after which half the population of mice from each group was sacrificed. The experiment was continued for another 3 weeks before the remaining mice were sacrificed. FRB supplementation could reduce the general observation of colitis and production of intestinal pro-inflammatory cytokines. FRB also increased intestinal mRNA levels of anti-inflammatory cytokine, tight junction, and anti-microbial proteins. Furthermore, FRB supplementation suppressed markers of intestinal fibrosis. This effect might have been achieved via the canonical Smad2/3 activation and the non-canonical pathway of activity. These results suggest that FRB may be an alternative therapeutic agent against inflammation-induced intestinal fibrosis.
已知发酵米糠(FRB)可保护小鼠肠道免受葡聚糖硫酸钠(DSS)诱导的炎症影响;然而,目前尚无关于补充FRB恢复结肠炎后肠道内稳态的报道。在本研究中,我们观察了饮食中补充FRB对DSS诱导的结肠炎后肠道恢复和纤维化发展的影响。将1.5%的DSS添加到小鼠饮用水中,持续5天。DSS处理结束后,立即处死8只小鼠。其余小鼠分为三组,分别给予以下饮食:对照组、10%米糠(RB)组和10%补充FRB组。饮食处理持续2周,之后每组处死一半的小鼠。实验再持续3周,然后处死其余小鼠。补充FRB可减轻结肠炎的总体表现并减少肠道促炎细胞因子的产生。FRB还增加了抗炎细胞因子、紧密连接蛋白和抗菌蛋白的肠道mRNA水平。此外,补充FRB可抑制肠道纤维化标志物。这种作用可能是通过经典的Smad2/3激活和非经典的活性途径实现的。这些结果表明,FRB可能是一种对抗炎症诱导的肠道纤维化的替代治疗剂。