Xiangdan injection mitigates cardiac injury in experimental sepsis through inflammatory suppression and mitochondrial...

Sepsis-induced myocardial injury (SIMI) is a major contributor to organ dysfunction and mortality in sepsis, driven primarily by excessive inflammation and mitochondrial dysfunction. Effective myocardial-targeted therapies remain limited. This study investigated the cardioprotective effects of Xiangdan injection in experimental sepsis induced by both Gram-positive and Gram-negative bacteria.

Sepsis was induced in male C57BL/6 mice by intraperitoneal injection of Staphylococcus aureus (Gram-positive) or Escherichia coli (Gram-negative). Xiangdan injection was administered at doses of 2.0, 2.5, and 5.0 ml/kg. Survival, myocardial histopathology, serum inflammatory cytokines, cardiac injury biomarkers, and mitochondrial ultrastructure were evaluated 12 h after sepsis induction. Mitochondrial damage was quantified using Flameng scoring.

Untreated sepsis significantly reduced survival (60% in Gram-positive and 70% in Gram-negative models) and caused severe myocardial injury. Xiangdan injection improved 12 h survival in a dose-dependent manner, achieving 100% survival at 5.0 ml/kg in both models. Sepsis markedly increased serum IL-6 (102.7 ± 13.6 pg/ml), TNF-α (98.5 ± 12.5 pg/ml), IL-1β (68.1 ± 8.9 pg/ml), and HMGB1 (3.5 ± 0.5 ng/ml), which were significantly reduced by Xiangdan injection at 5.0 ml/kg to 35.8 ± 5.2 pg/ml, 32.1 ± 5.3 pg/ml, 21.6 ± 3.8 pg/ml, and 1.1 ± 0.2 ng/ml, respectively (P < 0.01). Cardiac injury biomarkers BNP, CK-MB, and cTnI were also significantly decreased (BNP: 172.5 ± 22.1 to 62.2 ± 10.3 pg/ml; CK-MB: 398.7 ± 45.2 to 147.3 ± 19.4 U/L; cTnI: 1.12 ± 0.19 to 0.29 ± 0.06 ng/ml; P < 0.01). Mitochondrial ultrastructural damage was markedly attenuated, with Flameng scores reduced from 3.9 ± 0.5 to 1.5 ± 0.4 following high-dose Xiangdan treatment (P < 0.01).

Xiangdan injection significantly attenuated the sepsis-induced myocardial injury by suppressing systemic inflammation, reducing cardiac injury, and preserving myocardial mitochondrial integrity in a dose-dependent and pathogen-independent manner.