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亚麻籽低聚糖通过调节肠道微生物群和修复小鼠肠道屏障来减轻右旋糖酐硫酸钠诱导的结肠炎。

Flaxseed oligosaccharides alleviate DSS-induced colitis through modulation of gut microbiota and repair of the intestinal barrier in mice.

作者信息

Xu Zhenxia, Chen Wenchao, Deng Qianchun, Huang Qingde, Wang Xu, Yang Chen, Huang Fenghong

机构信息

Oil Crops Research Institute of the Chinese Academy of Agricultural Sciences, Oil Crops and Lipids Process Technology National & Local Joint Engineering Laboratory, Hubei Key Laboratory of Lipid Chemistry and Nutrition, Key Laboratory of Oilseeds Processing, Ministry of Agriculture and Rural Affairs, No. 2 Xudong 2nd Road, Wuhan 430062, China.

Huazhong Agricultural University, No. 1 Shizishan Street, Wuhan 430070, China.

出版信息

Food Funct. 2020 Sep 23;11(9):8077-8088. doi: 10.1039/d0fo01105c.

Abstract

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.

摘要

肠道上皮屏障功能障碍与肠道微生物群失调共同促成结肠炎的发生和发展。本研究旨在评估低聚亚麻籽糖(FOSs)对葡聚糖硫酸钠(DSS)诱导的溃疡性结肠炎(UC)小鼠的影响,并阐明其潜在机制。通过在饮用水中给予2% DSS 8天来诱导小鼠患UC。然后,通过灌胃给予FOS(50 mg kg-1 d-1、100 mg kg-1 d-1和200 mg kg-1 d-1),持续14天。结果表明,FOS治疗(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,显著改善了结肠炎。FOS治疗(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)显著抑制了促炎细胞因子的水平,包括肿瘤坏死因子(TNF)-α、白细胞介素(IL)-6和白细胞介素(IL)-1β,但增加了抗炎细胞因子白细胞介素(IL)-10的水平。16S rDNA基因高通量测序结果表明,FOS治疗增加了肠道微生物多样性,并抑制了炎症相关细菌(如未鉴定的梭菌目)的增殖。补充FOS还观察到总短链脂肪酸(SCFAs)、丙酸和丁酸增加。FOS(200 mg kg-1d-1)还通过增加Claudin1和Occludin的蛋白水平来保护肠道屏障。总之,FOS通过调节肠道微生物群和修复肠道屏障减轻了DSS诱导的结肠炎。

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