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Polysaccharides and glycosides from Aralia echinocaulis protect rats from arthritis by modulating the gut microbiota
Yunzhi Li1, Minxing Dai2, Lulu Wang2
1School of Pharmacy, Anhui University of Chinese Medicine, Hefei, Anhui, 230012, China; Anhui Province Key Laboratory of Chinese Medicinal Formula, Hefei, Anhui, 230012, China.
Ethnopharmacological Relevance:
Aralia echinocaulis has been used in traditional medicines in China and exhibits good effects on rheumatoid arthritis (RA).
Aim Of The Study:
Aralia echinocaulis is rich in polysaccharides and glycosides. This study aims to explore the effect of total polysaccharide and glycoside (TPG) from A. echinocaulis on an RA rat model and the role of alterations in gut microbes mediated by TPG.
Materials And Methods:
In this study, a collagen-induced arthritis (CIA) rat model was constructed and used to evaluate the effects of TPG in vivo. 16S rRNA sequencing was used to detect the changes in the gut microbiota. A cooccurrence analysis was conducted by calculating Spearman's rank correlations. Microbial functions were predicted using PICRUSt with the KEGG and COG databases.
Results:
The results showed that TPG from A. echinocaulis could inhibit arthritis, reduce serum IL-1β and TNF-α levels, and improve synovial pathology in the RA rat model but failed to produce the same results in a pseudoaseptic RA rat model. 16S rRNA sequencing verified that TPG could modulate the gut microbiota community structure of RA rats. The cooccurrence analysis found 19 out of the 50 most abundant genera in a cooccurrence network, of which 16 showed a positive correlation and 3 showed a negative correlation. KEGG pathway and COG function analyses found that TPG-induced alterations in the gut microbiota might be correlated with the circulatory system, excretory system, metabolic diseases, signaling molecules and interactions, coenzyme transport and metabolism, and nucleotide transport and metabolism.
Conclusions:
TPG from A. echinocaulis had significant effects on the RA rat model, which are related to the modulation of the gut microbiota. These results are useful to better understanding the mechanisms of TPG in RA.
