Remodeling the gut-heart axis: Danggui Sini granule mitigates vasospastic coronary heart disease via microbiota-metabolite interactions - Report - MDSpire

Remodeling the gut-heart axis: Danggui Sini granule mitigates vasospastic coronary heart disease via microbiota-metabolite interactions

  • By

  • Haipeng Tang

  • Zhiliang Sun

  • Shanshan Wang

  • Zhi Chen

  • Wenzhu Wang

  • Yang Wang

  • Jiyu Gong

  • Xiaoyan Xie

  • Wenyi Gao

  • May 22, 2026

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Clinical Report: Modulating the Gut-Heart Connection with Danggui Sini Granule

Overview

This study investigates the effects of Danggui Sini Granule (DSG) on vasospastic coronary heart disease (CHD) in a rat model. DSG demonstrated cardioprotective effects through modulation of gut microbiota, lipid metabolism, and inflammation pathways.

Background

Coronary heart disease (CHD) is a leading cause of morbidity and mortality globally, with persistent cardiovascular risk despite standard therapies. The gut-heart axis has emerged as a potential therapeutic target, as gut microbial dysbiosis can influence cardiovascular health. Understanding the mechanisms by which interventions like DSG affect this axis may enhance CHD management.

Data Highlights

ParameterEffect of DSG
ST-segment elevationAttenuated
Myocardial histopathological injuryReduced
Systemic inflammatory mediators (TNF-α, IL-6)Lowered
Opportunistic/pathogenic generaReduced
Beneficial taxa (Lactobacillus, Clostridium)Enriched

Key Findings

  • DSG reduced ST-segment elevation in a rat model of vasospastic CHD.
  • Histopathological injury to the myocardium was significantly mitigated by DSG treatment.
  • DSG lowered levels of systemic inflammatory markers, including TNF-α and IL-6.
  • Microbiota analysis revealed a reduction in pathogenic genera and an increase in beneficial taxa.
  • Metabolomics indicated restoration of protective lipid mediators associated with cardiovascular health.

Clinical Implications

The findings suggest that DSG may provide a multifaceted approach to managing vasospastic CHD by targeting gut microbiota and metabolic pathways. Further research is needed to validate these mechanisms and their clinical relevance.

Conclusion

DSG shows promise in providing cardioprotective effects in vasospastic CHD through gut-heart-axis modulation. Future studies should focus on establishing causal relationships in these observed effects.

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