School of Public Health, Guangdong Pharmaceutical University, Guangzhou 510310, China.
School of Food Science, Guangdong Pharmaceutical University, Zhongshan 528453, China.
Food Funct. 2020 Apr 30;11(4):2953-2968. doi: 10.1039/d0fo00178c.
Non-alcoholic fatty liver disease is associated with gut microbiota, oxidative stress, and inflammation. We aimed to investigate the possible mechanism by which noni fruit polysaccharide (NFP) improved hepatic oxidative stress and inflammation in rats under a high-fat diet (HFD) by modulating short-chain fatty acids (SCFAs), the intestinal barrier, and gut microbiota. Hepatic oxidative stress, inflammation, and gut dysbiosis in rats were induced through HFD feeding for 4 weeks, followed by intervention with NFP treatment (100 mg per kg bw) for 5 weeks. The results showed that NFP reduced body weight gain and improved lipid metabolism, hepatic oxidative stress, and inflammation in rats under a HFD. Aside from these beneficial effects, NFP positively affected the SCFA production and reversed the HFD-induced gut dysbiosis as indicated by improved microbiota diversity and composition. The levels of Lactobacillus, Ruminococcaceae_UCG_014, Parasutterella, [Eubacterium]_coprostanoligenes_group, and Ruminococcus_1 improved, whereas the levels of Prevotella_9, Collinsella, Bacteroides, and Turicibacter decreased. Furthermore, NFP maintained the colonic barrier integrity (increased the mRNA relative expression of CCL5, ZO-1, and occludin in the colon, and decreased the serum CCL5 level), and decreased the serum lipopolysaccharide level. Thus, NFP may modulate the gut microflora and SCFA production and reduce the permeability of the colonic barrier and metabolic endotoxemia, thereby alleviating hepatic oxidative stress and inflammation in rats under a HFD.
非酒精性脂肪性肝病与肠道微生物群、氧化应激和炎症有关。我们旨在通过调节短链脂肪酸（SCFAs）、肠道屏障和肠道微生物群，研究诺丽果多糖（NFP）改善高脂肪饮食（HFD）大鼠肝脏氧化应激和炎症的可能机制。通过 HFD 喂养 4 周诱导大鼠肝脏氧化应激、炎症和肠道菌群失调，然后用 NFP 治疗（100mg/kg bw）干预 5 周。结果表明，NFP 可降低 HFD 大鼠的体重增加，改善其脂质代谢、肝脏氧化应激和炎症。除了这些有益作用外，NFP 还积极影响 SCFA 的产生，并通过改善微生物多样性和组成来逆转 HFD 引起的肠道菌群失调。Lactobacillus、Ruminococcaceae_UCG_014、Parasutterella、[Eubacterium]_coprostanoligenes_group 和 Ruminococcus_1 的水平提高，而 Prevotella_9、Collinsella、Bacteroides 和 Turicibacter 的水平降低。此外，NFP 维持结肠屏障完整性（增加结肠中 CCL5、ZO-1 和 occludin 的 mRNA 相对表达，并降低血清 CCL5 水平），并降低血清脂多糖水平。因此，NFP 可能通过调节肠道微生物群和 SCFA 产生，降低结肠屏障的通透性和代谢性内毒素血症，从而减轻 HFD 大鼠的肝脏氧化应激和炎症。
