• 研究通过给予C57BL/6小鼠高脂肪和高糖饮食8周，诱导小鼠肝脂肪变性，然后口服壳寡糖溶液干预12周；
• 壳寡糖可以改善胰岛素抵抗和肝脂肪变性，降低脂质指数水平，减少脂质在肝脏中的积累，增强肝脏的抗氧化能力，缓解肝脏损伤和炎症；
• 壳寡糖可以显著提高有益菌群的丰度，降低有害菌群的丰度，提高肠道代谢物总量和短链脂肪酸水平，改变肠道菌群结构；
• 壳寡糖改善了回肠和结肠的LPS水平和屏障功能障碍，上调了结肠中ZO-1、occludin和claudin蛋白水平，下调了肝脏LPS/TLR4/NF-κB炎症通路；
• 总之，壳寡糖可以改善非酒精性脂肪肝的肠道菌群结构，调节炎症信号通路，从而缓解高糖高脂饮食诱导的肝内脂质积累。
   

来自广东药科大学天然产物与新药工程技术研究中心苏政权团队发表在Marine Drugs上的文章，发现壳寡糖通过改变肠道菌群结构和肠道屏障来调节LPS/TLR4/NF-κB炎症通路，最终影响NAFLD的进展。这项研究不仅为新型NAFLD药物的开发提供了理论依据和参考，为深入了解壳寡糖的分子机制提供了基础，也为海洋医药产品的研究提供了参考依据和广阔的发展前景。

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 Marine Drugs     [IF:6.085]

Marine Chitooligosaccharide Alters Intestinal Flora Structure and Regulates Hepatic Inflammatory Response to Influence Nonalcoholic Fatty Liver Disease

海洋来源的壳寡糖通过调整肠道菌群结构，调节肝脏炎症反应，改善非酒精性脂肪肝

10.3390/md20060383

06-07, Article

Abstract:
In this study, C57BL/6 mice were given an HFHSD diet for 8 weeks to induce hepatic steatosis and then given COSM solution orally for 12 weeks. The study found that the HFHSD diet resulted in steatosis and insulin resistance in mice. The formation of NAFLD induced by HFHSD diet was related to the imbalance of intestinal flora. However, after COSM intervention, the abundance of beneficial bacteria increased significantly, while the abundance of harmful bacteria decreased significantly. The HFHSD diet also induced changes in intestinal bacterial metabolites, and the content of short-chain fatty acids in cecal contents after COSM intervention was significantly higher than that in the model group. In addition, COSM not only improved LPS levels and barrier dysfunction in the ileum and colon but upregulated protein levels of ZO-1, occludin, and claudin in the colon and downregulated the liver LPS/TLR4/NF-kappaB inflammatory pathway. We concluded that the treatment of marine chitooligosaccharide COSM could improve the intestinal microflora structure of the fatty liver and activate an inflammatory signaling pathway, thus alleviating the intrahepatic lipid accumulation induced by HFHSD.

First Authors:
Jiayao Feng

Correspondence Authors:
Zhengquan Su

All Authors:
Jiayao Feng, Yongjian Liu, Jiajia Chen, Yan Bai , Jincan He, Hua Cao, Qishi Che, Jiao Guo, and Zhengquan Su