Xiangdan Injection attenuates experimental sepsis-induced myocardial injury by suppressing inflammation and preserving mitochondrial ultrastructure.

BACKGROUND

Sepsis-associated cardiac dysfunction is a major contributor to morbidity and mortality and is driven by dysregulated inflammation and impaired cellular bioenergetics. Therapeutic strategies that target both processes remain limited.

METHODS

This study evaluated the cardioprotective effects of Xiangdan Injection in murine sepsis models induced by Gram-positive Staphylococcus aureus and Gram-negative Escherichia coli.

RESULTS

Sepsis caused reduced survival, myocardial structural damage, increased circulating inflammatory mediators, elevated cardiac injury biomarkers, and mitochondrial ultrastructural disruption. Xiangdan Injection improved survival in a dose-dependent manner (p < 0.05), reduced serum IL-6, TNF-α, IL-1β, and HMGB1 levels (all p < 0.05), and decreased BNP, CK-MB, and cardiac troponin I levels (all p < 0.05). Transmission electron microscopy showed preservation of mitochondrial ultrastructure, reflected by reduced mitochondrial damage scores (p < 0.05).

CONCLUSION

These findings indicate that Xiangdan Injection attenuates sepsis-induced myocardial injury by suppressing systemic inflammation and preserving mitochondrial structure. Comparable effects were observed in both bacterial models, supporting further investigation of Xiangdan Injection as a potential adjunctive intervention for sepsis-associated myocardial injury.