Konjac Mannan Oligosaccharides enhanced intestinal barrier function to improve alcoholic nervous injury
- Author:
Jing-Jing CHEN
1
;
Wen-Yan ZHONG
1
;
Wen-Zhuo SHEN
1
;
Li XIAO
1
;
Cheng-Fu YUAN
1
;
Wen-Yan ZHONG
2
;
Li XIAO
2
;
Cheng-Fu YUAN
2
Author Information
- Publication Type:Journal Article
- Keywords: alcohol; konjac mannan oligosaccharides; LPS; Microglia; NLRP3 inflammasome; Occludin
- From: Chinese Pharmacological Bulletin 2024;40(3):447-454
- CountryChina
- Language:Chinese
- Abstract: Aim Excessive cerebral inflammation caused by chronic alcohol intake is an important risk factor for central nervous system injury. The purpose of this study was to explore the protective effect of konjac mannan oligosaccharide (KMOS) on central nervous system inflammation in alcohol-fed mice and its mechanism. Methods The chronic alcohol fed model of C57BL/6J mice was established using Gao-binge method. And the different doses of KMOS were gavaged every day for 6 weeks. The neuronal damage and microglia activation were evaluated in cerebral cortex and hippocampus. The damage of colon tissue was assessed and serum LPS concentrations were measured. In vitro, Caco-2 cells were stimulated with LPS to establish intestinal mucosal injury model. Results Chronic alcohol intake can cause brain neuron damage in mice, and different doses of KMOS effectively reduced the activation state of microglia, decreased the expression of inflammatory factors caused by the activation of the NLRP3 inflammasome and alleviated neuronal damage in the brain tissue of alcohol-fed mice. The results of colon tissue analysis showed that the use of KMOS effectively reduced the concentration of endotoxin LPS in serum of alcohol-fed mice, alleviated the pathological injury and inflammatory response of colon tissue, and enhanced the expression of Occludin in intestinal tissue. In vitro experiments also showed that KMOS significantly inhibited the inflammatory reaction of Caco-2 cells exposed to alcohol and increased the expression of Occludin protein. Conclusions KMOS treatment effectively inhibited intestinal inflammation caused by alcohol intake, repaired intestinal barrier to prevent the entry of intestinal LPS into brain tissue, decreased the activation of microglia, and then improved brain neuron damage. KMOS had the potential to prevent alcoholic nerve injury.
