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岩藻黄质可缓解葡聚糖硫酸钠诱导的小鼠结肠炎和肠道微生物失调。

Fucoxanthin Alleviates Dextran Sulfate Sodium-Induced Colitis and Gut Microbiota Dysbiosis in Mice.

机构信息

School of Food Science and Engineering, Qilu University of Technology (Shandong Academy of Sciences), No. 3501 Daxue Road, Jinan, Shandong 250353, China.

Shandong Haizhibao Ocean Science and Technology Co., Ltd., No. 259 Pinghai East Road, Rongcheng City, Shandong 264300, China.

出版信息

J Agric Food Chem. 2024 Feb 28;72(8):4142-4154. doi: 10.1021/acs.jafc.3c08811. Epub 2024 Feb 14.

Abstract

The purpose of this study was to evaluate the preventive role and underlying mechanisms of fucoxanthin (Fx) on dextran sulfate sodium (DSS)-induced colitis in mice. The present data demonstrated that oral administration of Fx (50 and 200 mg/kg body weight/day) for 36 days significantly alleviated the severity of colitis in DSS-treated mice, as evidenced by attenuating body weight loss, bloody stool, diarrhea, shortened colon length, colonic epithelium distortion, a thin mucus layer, goblet cell depletion, damaged crypts, and extensive infiltration of inflammatory cells in the colonic mucosa. Additionally, Fx notably relieved DSS-induced intestinal epithelial barrier dysfunction via maintaining the tight junction function and preventing excessive apoptosis of colonic epithelial cells. Moreover, Fx effectively diminished colonic inflammation and oxidative stress in DSS-treated mice, and its mechanisms might be due to blunting the activation of NF-κB and NLRP3 inflammasome signaling pathways. Furthermore, Fx also modulates DSS-induced gut microbiota dysbiosis via recovering the richness and diversity of gut microbiota and reshaping the structure of gut microbiota, such as increasing the and (F/B) ratio and elevating the relative abundance of some potential beneficial bacteria, including and . Overall, Fx might be developed as a promising functional ingredient to prevent colitis and maintain intestinal homeostasis.

摘要

本研究旨在评估岩藻黄质(Fx)对葡聚糖硫酸钠(DSS)诱导的小鼠结肠炎的预防作用及其潜在机制。目前的数据表明,Fx(50 和 200mg/kg 体重/天)连续口服 36 天可显著减轻 DSS 处理小鼠的结肠炎严重程度,表现为减轻体重减轻、血便、腹泻、缩短结肠长度、结肠上皮变形、薄粘液层、杯状细胞耗竭、隐窝损伤以及结肠黏膜中炎症细胞的广泛浸润。此外,Fx 还通过维持紧密连接功能和防止结肠上皮细胞过度凋亡,显著缓解 DSS 诱导的肠道上皮屏障功能障碍。此外,Fx 还能有效减轻 DSS 处理小鼠的结肠炎症和氧化应激,其机制可能与抑制 NF-κB 和 NLRP3 炎性体信号通路的激活有关。此外,Fx 还通过恢复肠道微生物群落的丰富度和多样性以及重塑肠道微生物群落的结构,例如增加 和 (F/B)比值并提高一些潜在有益细菌的相对丰度,如 和 ,来调节 DSS 诱导的肠道微生物群落失调。总的来说,Fx 可能被开发为一种有前途的功能性成分,以预防结肠炎和维持肠道内稳态。

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