# Attenuation of sepsis-induced myocardial injury by Xiangdan injection via mitochondrial protection and inflammation suppression in mice

**Authors:** Yuejin Chang, Wenlei Zhang, Jinbo Pan, Zhenhao Lin, Hongxia Bai, Hui Li

PMC · DOI: 10.3389/fmed.2025.1669474 · Frontiers in Medicine · 2025-11-07

## TL;DR

Xiangdan injection protects the heart in sepsis by reducing inflammation and preserving mitochondria in mice.

## Contribution

Xiangdan injection shows dose-dependent cardioprotective effects in sepsis through mitochondrial protection and inflammation suppression.

## Key findings

- Xiangdan injection improved survival and reduced inflammatory cytokines in septic mice.
- It preserved mitochondrial integrity and reduced cardiac injury markers dose-dependently.
- The effects align with modulation of TLR4/NF-κB and JAK2/STAT3 pathways.

## Abstract

Sepsis-induced myocardial injury (SIMI) is a leading cause of organ dysfunction and mortality in septic patients. Effective myocardial-protective therapies remain limited.

This study evaluated the cardioprotective effects of Xiangdan injection in murine SIMI models caused by both Gram-positive and Gram-negative bacteria.

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.

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 (P < 0.05).

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.

## Linked entities

- **Proteins:** TLR4 (toll like receptor 4), NFKB1 (nuclear factor kappa B subunit 1), JAK2 (Janus kinase 2), STAT3 (signal transducer and activator of transcription 3)
- **Species:** Mus musculus (taxon 10090)

## Full-text entities

- **Genes:** Nfkb1 (nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105) [NCBI Gene 18033] {aka NF-KB1, NF-kappaB, NF-kappaB1, p105, p50, p50/p105}, Tlr4 (toll-like receptor 4) [NCBI Gene 21898] {aka Lps, Ly87, Ran/M1, Rasl2-8}, Stat3 (signal transducer and activator of transcription 3) [NCBI Gene 20848] {aka 1110034C02Rik, Aprf}, Jak2 (Janus kinase 2) [NCBI Gene 16452] {aka Fd17}
- **Diseases:** septic (MESH:D001170), organ dysfunction (MESH:D009102), myocardial injury (MESH:D009202), SIMI (MESH:D018805), cardiac injury (MESH:D006331), inflammation (MESH:D007249)
- **Species:** Mus musculus (house mouse, species) [taxon 10090], Homo sapiens (human, species) [taxon 9606], Bacteria Latreille et al. 1825 (Bacteria stick insect, genus) [taxon 629395]
- **Cell lines:** /6 — Homo sapiens (Human), Tongue squamous cell carcinoma, Cancer cell line (CVCL_5985)

## Full text

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## Figures

11 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12634624/full.md

## References

36 references — full list in the complete paper: https://tomesphere.com/paper/PMC12634624/full.md

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Source: https://tomesphere.com/paper/PMC12634624