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Flaxseed oligosaccharides alleviate DSS-induced colitis through modulation of gut microbiota and repair of the intestinal barrier in mice.
Food & Function ( IF 5.1 ) Pub Date : 2020-07-28 , DOI: 10.1039/d0fo01105c Zhenxia Xu 1 , Wenchao Chen 1 , Qianchun Deng 1 , Qingde Huang 1 , Xu Wang 2 , Chen Yang 1 , Fenghong Huang 3
Food & Function ( IF 5.1 ) Pub Date : 2020-07-28 , DOI: 10.1039/d0fo01105c Zhenxia Xu 1 , Wenchao Chen 1 , Qianchun Deng 1 , Qingde Huang 1 , Xu Wang 2 , Chen Yang 1 , Fenghong Huang 3
Affiliation
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Intestinal epithelial barrier dysfunction with dysbiosis of gut microbiota contributes to the occurrence and acceleration of colitis. This study aimed to evaluate the effect of flaxseed oligosaccharides (FOSs) on dextran sulfate sodium (DSS)-induced ulcerative colitis (UC) mice and to elucidate the underlying mechanisms. UC was induced in mice by administering 2% DSS in drinking water for 8 days. Then, FOS (50 mg kg−1 d−1, 100 mg kg−1 d−1 and 200 mg kg−1 d−1) was administered by gavage for 14 days. The results showed that FOS treatment (200 mg kg−1 d−1) significantly ameliorated colitis by decreasing disease activity index (DAI), increasing colon length and improving colonic histology. FOS treatment (200 mg kg−1 d−1) down-regulated the critical markers of oxidative stresses, including malondialdehyde (MDA) and myeloperoxidase (MPO). Furthermore, FOS (200 mg kg−1 d−1) significantly suppressed the levels of pro-inflammatory cytokines including tumor necrosis factor (TNF)-α, interleukin (IL)-6 and interleukin (IL)-1β but increased that of anti-inflammatory cytokine interleukin (IL)-10. The 16S rDNA gene high-throughput sequencing results indicated that FOS treatment increased the gut microbial diversity and inhibited the proliferation of inflammation-related bacteria such as unidentified_Clostridiales. An increase in total short-chain fatty acids (SCFAs), propionic acid and butyric acid, was also observed by FOS supplementation. FOS (200 mg kg−1d−1) also protected the intestinal barrier by increasing the protein levels of Claudin1 and Occludin. In conclusion, FOS attenuated DSS-induced colitis by modulating the gut microbiota and repairing the intestinal barrier.
中文翻译：
亚麻籽低聚糖通过调节肠道菌群和修复小鼠肠道屏障来缓解DSS诱导的结肠炎。
肠道上皮屏障功能紊乱和肠道菌群失调有助于结肠炎的发生和加速。这项研究旨在评估亚麻籽寡糖（FOSs）对硫酸葡聚糖钠（DSS）诱导的溃疡性结肠炎（UC）小鼠的影响，并阐明其潜在机制。通过在饮用水中施用2％DSS持续8天，在小鼠中诱发UC。然后，通过管饲法施用FOS（50mg kg -1 d -1，100mg kg -1 d -1和200mg kg -1 d -1）14天。结果表明FOS处理（200 mg kg -1 d -1）通过降低疾病活动指数（DAI），增加结肠长度和改善结肠组织学来显着改善结肠炎。FOS处理（200 mg kg -1 d -1）下调了氧化应激的关键标志物，包括丙二醛（MDA）和髓过氧化物酶（MPO）。此外，FOS（200 mg kg -1 d -1）显着抑制促炎细胞因子的水平，包括肿瘤坏死因子（TNF）-α，白介素（IL）-6和白介素（IL）-1β，但增加了抗炎症因子的水平。 -炎症细胞因子白介素（IL）-10。16S rDNA基因高通量测序结果表明，FOS处理可增加肠道微生物的多样性，并抑制炎症相关细菌的繁殖，例如unidentified_Clostridiales。通过FOS补充，总短链脂肪酸（SCFA），丙酸和丁酸也有所增加。FOS（200 mg kg -1 d -1）还通过增加Claudin1和Occludin的蛋白质水平来保护肠道屏障。总之，FOS通过调节肠道菌群和修复肠屏障来减轻DSS诱导的结肠炎。
更新日期：2020-09-23
中文翻译：
亚麻籽低聚糖通过调节肠道菌群和修复小鼠肠道屏障来缓解DSS诱导的结肠炎。
肠道上皮屏障功能紊乱和肠道菌群失调有助于结肠炎的发生和加速。这项研究旨在评估亚麻籽寡糖（FOSs）对硫酸葡聚糖钠（DSS）诱导的溃疡性结肠炎（UC）小鼠的影响，并阐明其潜在机制。通过在饮用水中施用2％DSS持续8天，在小鼠中诱发UC。然后，通过管饲法施用FOS（50mg kg -1 d -1，100mg kg -1 d -1和200mg kg -1 d -1）14天。结果表明FOS处理（200 mg kg -1 d -1）通过降低疾病活动指数（DAI），增加结肠长度和改善结肠组织学来显着改善结肠炎。FOS处理（200 mg kg -1 d -1）下调了氧化应激的关键标志物，包括丙二醛（MDA）和髓过氧化物酶（MPO）。此外，FOS（200 mg kg -1 d -1）显着抑制促炎细胞因子的水平，包括肿瘤坏死因子（TNF）-α，白介素（IL）-6和白介素（IL）-1β，但增加了抗炎症因子的水平。 -炎症细胞因子白介素（IL）-10。16S rDNA基因高通量测序结果表明，FOS处理可增加肠道微生物的多样性，并抑制炎症相关细菌的繁殖，例如unidentified_Clostridiales。通过FOS补充，总短链脂肪酸（SCFA），丙酸和丁酸也有所增加。FOS（200 mg kg -1 d -1）还通过增加Claudin1和Occludin的蛋白质水平来保护肠道屏障。总之，FOS通过调节肠道菌群和修复肠屏障来减轻DSS诱导的结肠炎。
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