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

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 ( < 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 ( < 0.05,  < 0.01), and vasoactive intestinal peptide (VIP) was reduced by SMY ( < 0.01) compared with MC. Furthermore, alpha diversity was significantly decreased in the model rats compared to the normal rats ( < 0.05) and increased with SMY treatment ( < 0.01). The most abundant phyla were and , followed by , , and . At the genus level, there was a lower relative abundance of , , , and , and a higher relative abundance of , and in the MC group The relative abundance of , , , , , , , , , , and 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 was negatively correlated with the change in GAS, and positively correlated with the change in VIP ( < 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.