Serum, spleen metabolomics and gut microbiota reveals effect of catalpol on blood deficiency syndrome caused by cyclophosphamide and acetylphenylhydrazine.

Catalpol (CA), extracted from Rehmannia Radix, holds extensive promise as a natural medicinal compound. This study employed 16S rRNA gene sequencing and combined serum and spleen metabolomics to profoundly investigate the therapeutic effects of CA on blood deficiency syndrome (BDS) and the underlying mechanisms. Notably, CA exhibited effectiveness against BDS induced by cyclophosphamide (CP) and acetylphenylhydrazine (APH) in rats-CA substantially elevated levels of crucial indicators such as erythropoietin (EPO), granulocyte colony-stimulating factor (G-CSF), tumor necrosis factor-alpha (TNF-a), and interleukin-6 (IL-6). Additionally, CA could alleviate peripheral blood cytopenia. Furthermore, the analysis of 16S rRNA revealed that CA had the potential to reverse the Firmicutes/Bacteroidetes (F/B) ratio associated with BDS. Through comprehensive serum and spleen metabolomic profiling, we successfully identified 22 significant biomarkers in the serum and 23 in the spleen, respectively. Enrichment analysis underscored Glycerophospholipid metabolism and Sphingolipid metabolism as potential pathways through which CA exerts its therapeutic effects on BDS.