Ginsenoside Rh4 alleviates antibiotic-induced intestinal inflammation by regulating the TLR4-MyD88-MAPK pathway and gut microbiota composition.

Abstract

Ginsenoside Rh4, as a bioactive component obtained from Panax notoginseng, has excellent pharmacological properties. However, its role in regulating gut microbiota and intestinal inflammation is still poorly understood. Thus, the aim of this study is to investigate the effect of Rh4 on gut microbiota, especially antibiotic-induced microbiota perturbation, and the underlying mechanisms. C57BL/6 mice were given different doses of Rh4 after the establishment of a gut microbiota disturbance model with antibiotics. Our data revealed that Rh4 administration could greatly improve the pathological phenotype, gut barrier disruption, and intestinal inflammation in mice that had been antibiotic-induced. Notably, it was found that Rh4 significantly inhibited the TLR4-MyD88-MAPK signaling pathway. In addition, Rh4 treatment could significantly increase the number of short chain fatty acids (SCFAs) and bile acids (BAs). These changes were accompanied with beneficial alterations in gut microbiota diversity and composition. In conclusion, Rh4 improves intestinal inflammation and induces potentially beneficial changes in the gut microbiota, which are conducive to revealing host-microbe interactions.

• Authors: Xue Bai , Rongzhan Fu , Zhiguang Duan , Yannan Liu , Chenhui Zhu , Daidi Fan
• Journal: Food & function (Food Funct) Vol. 12 Issue 7 Pg. 2874-2885 (Apr 07 2021) ISSN: 2042-650X [Electronic] England
• PMID: 33877243 (Publication Type: Journal Article)

Chemical References

• Anti-Bacterial Agents
• Cytokines
• Fatty Acids, Volatile
• Ginsenosides
• Myd88 protein, mouse
• Myeloid Differentiation Factor 88
• Tlr4 protein, mouse
• Toll-Like Receptor 4
• ginsenoside Rh4
• Mitogen-Activated Protein Kinases

Topics

• Animals
• Anti-Bacterial Agents (adverse effects)
• Colitis (chemically induced, drug therapy, physiopathology)
• Cytokines (metabolism)
• Dysbiosis (chemically induced, drug therapy)
• Fatty Acids, Volatile (analysis)
• Feces (chemistry)
• Gastrointestinal Microbiome (drug effects, physiology)
• Ginsenosides (administration & dosage)
• Male
• Mice
• Mice, Inbred C57BL
• Mitogen-Activated Protein Kinases (metabolism)
• Myeloid Differentiation Factor 88 (metabolism)
• Permeability (drug effects)
• Signal Transduction (drug effects)
• Toll-Like Receptor 4 (metabolism)