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 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.