Work

Exploring the protective mechanism of Huangqishengmaiyin against anthracycline-induced cardiotoxicity in breast cancer with concomitant gut microbiota modulation

Year: 2026

Type: article

Abstract: Objective To elucidate the bioactive compounds and cardioprotective mechanism of Huangqishengmaiyin (HQSMY) against anthracycline-induced cardiotoxicity (AIC) in breast cancer with concomitant gut microbiota modulation. Methods Myocardial fibrosis was quantified using Masson's trichrome staining. Hematoxylin and eosin staining was used for general histopathological evaluation. Ultra-high-performance liquid chromatography-tandem mass spectrometry (UHPLC-Q Exactive HFX) was employed to comprehensively identify blood components in HQSMY. The regulatory effect of HQSMY on the gut microbiota of AIC mice was assessed by 16S rRNA microbial sequencing. Network pharmacology and molecular docking mapped the compound-target-pathway network. Western blot was performed to detect key proteins in the predicted pathways, including JAK1, STAT3, and HIF-1 α . Results HQSMY reduced myocardial fibrosis rates, enhanced gut microbiota diversity, abundance and health indices. Meanwhile, HQSMY increased the abundance of anti-inflammatory bacteria like Bacteroidetes and restored normal metabolic pathways in multiple gut microbes, including glycolysis. 42 blood components were identified, exhibiting antioxidant, anti-inflammatory, and gut microbiota-regulating activities. Network pharmacology analysis revealed that the JAK-STAT and HIF-1 signaling pathways are key mechanisms. Enrichment analysis focused on energy metabolism and inflammatory response. Western blot results confirmed that HQSMY significantly downregulated JAK1 and HIF-1 α protein expression; STAT3 was decreased without reaching statistical significance. Conclusion The components of HQSMY exhibit anti-inflammatory effects in myocardial tissue, meanwhile enhancing beneficial gut bacteria in intestine. The regulatory effect of HQSMY may be exerted through JAK-STAT and HIF-1 pathways, as confirmed by altered expression of key proteins in these pathways.

Source: Frontiers in Cardiovascular Medicine

DOI: 10.3389/fcvm.2026.1818551