Abstract
Background: Diarrhea-predominant irritable bowel syndrome (D-IBS) is a clinically common functional intestinal disease, classified into "diarrhea," "abdominal pain," and "depression syndrome" categories according to traditional Chinese medicine (TCM). The exact pathogenesis of D-IBS is still not fully understood. Gut microbiota regulates gastrointestinal nerve, endocrine, and immune functions and maintains gastrointestinal homeostasis through interaction with the brain-gut axis. In this study, we assessed the changes in gut microbiota in a D-IBS rat model with liver depression, spleen deficiency, and liver depression and spleen deficiency syndrome. We also discussed the biological basis of liver depression and spleen deficiency syndrome and the associations among the three syndromes from the perspective of gut microbiota. Methods: Ninety rats were divided into nine groups randomly: normal group (ZC), spleen deficiency syndrome groups (four PX groups), liver depression syndrome groups (two GY groups), and liver depression and spleen deficiency syndrome groups (two GYPX groups). The abdominal wall withdrawal reflex (AWR) test detected visceral sensitivity, while changes in gut microbiota were analyzed using 16S rRNA sequencing. Results: The visceral sensitivity of rats in the model group was significantly higher than that in the ZC group, and the visceral sensitivity of the GYPX groups was significantly higher compared to the PX and GY groups. 16S rRNA sequencing analysis showed that the D-IBS model gut microbiota's species number, alpha diversity, and beta diversity were changed; the Bacteroidota increased, and the Firmicutes decreased in the model group. The abundance of pathogenic bacteria, such as Bacteroidales, significantly increased in the GYPX groups compared to other groups. Conclusion: Oral administration of senna combined with restraint stress had different effects on visceral hypersensitivity, gut microbiota composition, and metabolic pathways in rats with D-IBS liver depression and spleen deficiency syndrome, and the liver depression factors play an important role in the pathogenesis of liver depression and spleen deficiency syndrome in D-IBS.