Shengmai Yin formula modulates the gut microbiota of spleen-deficiency rats

Abstract

Background Spleen-deficiency syndrome, an important pathological change in traditional Chinese medicine, has been proven to attribute to intestinal dysbacteriosis. Shengmai Yin (SMY), a classic formula for replenishing qi and restoring pulse, is a common medicine for critical emergencies in traditional Chinese Medicine. Interestingly, our previous study established a spleen-deficiency rat model and verified the potency of SMY formula in curing spleen-deficiency rats. Our goal herein was to explore whether SMY can modulate the composition of intestinal flora and alleviate spleen-deficiency in rats. Methods This experiment was randomly divided into three groups, namely the normal control group (NC), model control group (MC), and the Shengmai Yin group (SMY). After the treatment, the weight and symptom indexes of the rats were recorded, histological changes in the colon were observed, levels of serum D-xylose, gastrin (GAS), and vasoactive intestinal peptide (VIP) were measured, and gut microbiota profiling was conducted by 16S rRNA sequencing. Results The body mass of the spleen-deficiency model rats significantly decreased compared with that of the NC group, and SMY treatment significantly increased body mass compared with the MC group (P < 0.01). Colon histopathology revealed that SMY treatment alleviated colonic mucosal damage in spleen-deficiency rats. The serum levels of D-xylose and gastrin (GAS) were significant increased by SMY (P < 0.05, P < 0.01), and vasoactive intestinal peptide (VIP) was reduced by SMY (P < 0.01) compared with MC. Furthermore, alpha diversity was significantly decreased in the model rats compared to the normal rats (P < 0.05) and increased with SMY treatment (P < 0.01). The most abundant phyla were Firmicutes and Bacteroidetes, followed by Proteobacteria, Verrucomicrobia, and Actinobacteria. At the genus level, there was a lower relative abundance of Lactobacillus, Bacteroides, Akkermasia, and Allobaculum, and a higher relative abundance of Lachnospiraceae NK4A 136 group, Ruminococcaceae UCG-014, and Sphingomonas in the MC group. The relative abundance of Actinobacteria, Alistipes, Bifidobacterium, Bifidobacterium, Bifidobacteriaceae, Lachnospiraceae NK4A136group, Lactobacillus, Lactobacillaceae, Bacilli, Verrucomicrobiae, and Akkermansia were significantly abundant in the treatment groups, and thus may be singled out as potential biomarkers for SMY in the treatment of spleen deficiency. In addition, analysis on the correlation between species and physicochemical indexes showed that the abundance of Parasutterella was negatively correlated with the change in GAS, and positively correlated with the change in VIP (P < 0.01). Conclusion Our findings have provided preliminary evidence that modulating the gut microbiota may play a role in the treatment of spleen deficiency with SMY. However, further studies are needed to clarify the mechanism by which SMY regulation of related gut microbiota occurs.

Codonopsis pilosula Polysaccharide Improved Spleen Deficiency in Mice by Modulating Gut Microbiota and Energy Related Metabolisms

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Paeonol for the Treatment of Atherosclerotic Cardiovascular Disease: A Pharmacological and Mechanistic Overview

“…Previous studies have confirmed that natural medicines can be used for the treatment of a variety of intestinal and digestive system diseases by regulating intestinal flora (124,125). Intestinal flora plays an important role in the treatment of cardiovascular diseases using natural compounds (126).…”

Elucidation of the Reinforcing Spleen Effect of Jujube Fruits Based on Metabolomics and Intestinal Flora Analysis

“…( Chen et al., 2019 ; Liu et al., 2019 ; Ji et al., 2020 ; Qi et al., 2020 ). Spleen deficiency is also considered to be closely related to the imbalance of intestinal flora ( You et al., 2020 ). Therefore, exploring and revealing the relationship between metabolomics and structural alterations of intestinal flora of spleen deficiency can not only enrich and improve the essence of spleen deficiency, but also provide means to discover drugs for treating spleen deficiency and clarify its molecular mechanism.…”