ArticleFrontiers in medicine2025
Attenuation of sepsis-induced myocardial injury by Xiangdan injection via mitochondrial protection and inflammation suppression in mice.
Article in Frontiers in medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Xiangdan Injection attenuates experimental sepsis-induced myocardial injury by suppressing inflammation and preserving mitochondrial ultrastructure.Frontiers in pharmacology · 2026Article
- Xiangdan injection mitigates cardiac injury in experimental sepsis through inflammatory suppression and mitochondrial protection.Frontiers in medicine · 2026Article
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Authors and funding
6 authors.
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Abstract
Background: Sepsis-induced myocardial injury (SIMI) is a leading cause of organ dysfunction and mortality in septic patients. Effective myocardial-protective therapies remain limited. Objective: This study evaluated the cardioprotective effects of Xiangdan injection in murine SIMI models caused by both Gram-positive and Gram-negative bacteria. Methods: Male C57BL/6 mice were assigned to sham, sepsis, and three Xiangdan dose groups for each bacterial model using a randomization schedule. Xiangdan injection was administered by oral gavage 12 h before and immediately after bacterial challenge (prophylaxis/early intervention). Outcomes included survival, serum inflammatory cytokines, cardiac biomarkers, histopathology, and ultrastructural mitochondrial integrity. Results: Xiangdan injection markedly improved survival, reduced inflammatory cytokines and cardiac biomarkers, ameliorated myocardial histopathology, and preserved mitochondrial integrity in a dose-dependent manner in both sepsis models ( Conclusion: Xiangdan injection conferred robust cardioprotection in sepsis, combining anti-inflammatory effects, reduction of cardiac injury markers, and preservation of mitochondrial structure. These outcomes are consistent with the known capacity of traditional Chinese medicine formulations to modulate TLR4/NF-κB and JAK2/STAT3 pathways, thereby supporting mechanistic suppression of these cascades in our model.
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