文献类型： 外文期刊

作者： Lv, Wei-jie ¹ ; Liu, Cui ¹ ; Yu, Lin-zeng ² ; Zhou, Jia-hao ¹ ; Li, Yue ¹ ; Xiong, Ying ¹ ; Guo, Ao ¹ ; Chao, Li-min ¹ ; Qu, ¹ ;

作者机构： 1.South China Agr Univ, Guangdong Lab Lingnan Modern Agr, Guangdong Technol Res Tradit Chinese Vet Med & Na, Coll Vet Med, Guangzhou 510642, Guangdong, Peoples R China

2.Guangdong Acad Agr Sci, Inst Anim Hlth, Guangzhou 510640, Guangdong, Peoples R China

3.South China Agr Univ, Coll Anim Med, Guangzhou 510642, Guangdong, Peoples R China

4.Chinese Acad Sci, Key Lab Agroecol Proc Subtrop Reg, Hunan Prov Key Lab Anim Nutr Physiol & Metab Proc, Inst Subtrop Agr, Changsha, Hunan, Peoples R China

期刊名称：OXIDATIVE MEDICINE AND CELLULAR LONGEVITY （ 影响因子：6.543； 五年影响因子：7.454 ）

ISSN： 1942-0900

年卷期： 2020 年 2020 卷

页码：

收录情况： SCI

摘要： There is a bidirectional relationship between inflammatory bowel disease (IBD) and depression/anxiety. Emerging evidences indicate that the liver may be involved in microbiota-gut-brain axis. This experiment focused on the role of melatonin in regulating the gut microbiota and explores its mechanism on dextran sulphate sodium- (DSS-) induced neuroinflammation and liver injury. Long-term DSS-treatment increased lipopolysaccharide (LPS), proinflammation cytokines IL-1 beta and TNF-alpha, and gut leak in rats, breaking blood-brain barrier and overactivated astrocytes and microglia. Ultimately, the rats showed depression-like behavior, including reduction of sucrose preference and central time in open field test and elevation of immobility time in a forced swimming test. Oral administration with melatonin alleviated neuroinflammation and depression-like behaviors. However, melatonin supplementation did not decrease the level of LPS but increase short-chain fatty acid (SCFA) production to protect DSS-induced neuroinflammation. Additionally, western blotting analysis suggested that signaling pathways farnesoid X receptor-fibroblast growth factor 15 (FXR-FGF 15) in gut and apoptosis signal-regulating kinase 1 (ASK1) in the liver overactivated in DSS-treated rats, indicating liver metabolic disorder. Supplementation with melatonin markedly inhibited the activation of these two signaling pathways and its downstream p38. As for the gut microbiota, we found that immune response- and SCFA production-related microbiota, likeLactobacillusandClostridiumsignificantly increased, while bile salt hydrolase activity-related microbiota, likeStreptococcusandEnterococcus, significantly decreased after melatonin supplementation. These altered microbiota were consistent with the alleviation of neuroinflammation and metabolic disorder. Taken together, our findings suggest melatonin contributes to reshape gut microbiota and improves inflammatory processes in the hippocampus (HPC) and metabolic disorders in the liver of DSS rats.