Key result
Huangqishengmaiyin reduces anthracycline cardiotoxicity and myocardial fibrosis in mice via JAK1 and HIF-1α signaling.
Why the study?
The cardioprotective mechanism of Huangqishengmaiyin against anthracycline-induced cardiotoxicity in breast cancer with gut microbiota modulation was unclear.
Does Huangqishengmaiyin reduce myocardial fibrosis and modulate gut microbiota in a doxorubicin-induced cardiotoxicity breast cancer mouse model?
Does Huangqishengmaiyin reduce myocardial fibrosis and modulate gut microbiota in a doxorubicin-induced cardiotoxicity breast cancer mouse model?
Huangqishengmaiyin demonstrates cardioprotective effects against anthracycline-induced cardiotoxicity in a preclinical model, potentially mediated through gut microbiota modulation and the JAK-STAT and HIF-1 pathways.
Hypothesis-generating for anthracycline cardiotoxicity; human trials required before any clinical consideration.
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.
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Wang et al. (2026) studied Anthracycline-induced cardiotoxicity in breast cancer (n=25). Huangqishengmaiyin (HQSMY) vs. Doxorubicin only (Model group) and Dexrazoxane (Dex) was evaluated on Myocardial fibrosis rate. Huangqishengmaiyin alleviated anthracycline-induced myocardial fibrosis and cardiotoxicity in mice while enhancing gut microbiota diversity and downregulating JAK1 and HIF-1α signaling pathways.
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