College of Food Science and Engineering, Northwest A&F University, Yangling, P. R. China.
Institute of Wolfberry Engineering Technology Research, Ningxia Academy of Agricultural and Forestry Sciences, Yinchuan, P. R. China.
Mol Nutr Food Res. 2021 Apr;65(8):e2000745. doi: 10.1002/mnfr.202000745. Epub 2021 Mar 11.
Gut barrier dysfunction and inflammation originating from a dysbiotic gut microbiota (GM) are strongly associated with a high-fat diet (HFD). Anthocyanins from Lycium ruthenicum (ACs) show antiobesity effects through modulating the GM. However, the mechanism linking the antiobesity effects of ACs and GM modulation remains obscure.
To investigate the ameliorative effects of ACs on colonic barrier dysfunction and inflammation, mice are fed an HFD with or without ACs at doses of 50, 100, and 200 mg kg for 12 weeks. AC supplementation reduced weight gain, enriched short-chain fatty acid (SCFA)-producing bacteria (e.g., Ruminococcaceae, Muribaculaceae, Akkermansia, Ruminococcaceae_UCG-014, and Bacteroides) and SCFA content, depleted endotoxin-producing bacteria (e.g., Helicobacter and Desulfovibrionaceae), and decreased endotoxin (i.e., lipopolysaccharide) levels. SCFAs substantially activated G protein-coupled receptors (GPRs), inhibited histone deacetylases (HDAC), increased intestinal tight junction mRNA and protein expression levels, reduced intestinal permeability, and protected intestinal barrier integrity in HFD-induced mice. These effects mitigate intestinal inflammation by inhibiting the LPS/NF-κB/TLR4 pathway.
These data indicates that ACs can mitigate colonic barrier dysfunction and inflammation, induce SCFA production and inhibit endotoxin production by modulating the GM in HFD-fed mice. This finding provides a clue for understanding the antiobesity effects of ACs.
源自肠道菌群失调的肠道屏障功能障碍和炎症与高脂肪饮食(HFD)密切相关。黑果枸杞花色苷(ACs)通过调节肠道菌群(GM)显示出抗肥胖作用。然而,AC 调节 GM 与抗肥胖作用之间的联系机制尚不清楚。
为了研究 ACs 对结肠屏障功能障碍和炎症的改善作用,将小鼠用 HFD 喂养,并用 50、100 和 200mg/kg 的剂量补充 AC 12 周。AC 补充减少了体重增加,丰富了短链脂肪酸(SCFA)产生菌(例如,瘤胃菌科、黏液杆菌科、阿克曼氏菌、瘤胃菌科_UCG-014 和拟杆菌)和 SCFA 含量,减少了内毒素产生菌(例如,幽门螺杆菌和脱硫弧菌科),并降低了内毒素(即脂多糖)水平。SCFAs 可显著激活 G 蛋白偶联受体(GPR),抑制组蛋白去乙酰化酶(HDAC),增加肠紧密连接 mRNA 和蛋白表达水平,降低肠道通透性,并保护 HFD 诱导的小鼠的肠道屏障完整性。这些作用通过抑制 LPS/NF-κB/TLR4 途径减轻肠道炎症。
这些数据表明,ACs 可通过调节 HFD 喂养小鼠的 GM 来减轻结肠屏障功能障碍和炎症,诱导 SCFA 产生并抑制内毒素产生。这一发现为理解 ACs 的抗肥胖作用提供了线索。