香丹注射液通过炎症抑制和线粒体保护减轻实验性败血症的心脏损伤
Xiangdan injection mitigates cardiac injury in experimental sepsis through inflammatory suppression and mitochondrial protection.
摘要(中文译文)
脓毒症诱导的心肌损伤（SIMI）是脓毒症器官功能障碍和死亡的主要原因，主要由过度炎症和线粒体功能障碍驱动。有效的心肌靶向治疗仍然有限。本研究探讨了香丹注射液对革兰阳性菌和革兰阴性菌诱导的实验性脓毒症的心脏保护作用。通过腹腔注射（革兰阳性菌）或（革兰阴性菌）在雄性C57BL/6小鼠中诱导脓毒症。香丹注射液以2.0、2.5和5.0 ml/kg的剂量给药。在脓毒症诱导后12小时评估生存率、心肌组织病理学、血清炎性细胞因子、心脏损伤生物标志物和线粒体超微结构。使用Flameng评分对线粒体损伤进行定量。未治疗的脓毒症显著降低生存率（革兰阳性模型为60%，革兰阴性模型为70%）并导致严重心肌损伤。香丹注射液以剂量依赖性方式提高12小时生存率，在两种模型中5.0 ml/kg剂量均达到100%生存率。脓毒症显著升高血清IL-6（102.7 ± 13.6 pg/ml）、TNF-α（98.5 ± 12.5 pg/ml）、IL-1β（68.1 ± 8.9 pg/ml）和HMGB1（3.5 ± 0.5 ng/ml），香丹注射液5.0 ml/kg显著降低上述指标至35.8 ± 5.2 pg/ml、32.1 ± 5.3 pg/ml、21.6 ± 3.8 pg/ml和1.1 ± 0.2 ng/ml（< 0.01）。心脏损伤生物标志物BNP、CK-MB和cTnI也显著降低（BNP：172.5 ± 22.1降至62.2 ± 10.3 pg/ml；CK-MB：398.7 ± 45.2降至147.3 ± 19.4 U/L；cTnI：1.12 ± 0.19降至0.29 ± 0.06 ng/ml；< 0.01）。线粒体超微结构损伤明显减轻，高剂量香丹治疗后Flameng评分从3.9 ± 0.5降至1.5 ± 0.4（< 0.01）。香丹注射液通过抑制全身炎症、减轻心脏损伤和保护心肌线粒体完整性，以剂量依赖性和病原体非依赖性方式显著减轻脓毒症诱导的心肌损伤。
Abstract
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 (Gram-positive) or (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 ( < 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; < 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 ( < 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.
如何引用
AMA
Jingyu Xu. Xiangdan injection mitigates cardiac injury in experimental sepsis through inflammatory suppression and mitochondrial protection.. Frontiers in medicine. 2026; doi:10.3389/fmed.2026.1801630.
APA
Jingyu Xu (2026). Xiangdan injection mitigates cardiac injury in experimental sepsis through inflammatory suppression and mitochondrial protection.. Frontiers in medicine. https://doi.org/10.3389/fmed.2026.1801630
GB/T 7714
Jingyu Xu. Xiangdan injection mitigates cardiac injury in experimental sepsis through inflammatory suppression and mitochondrial protection.[J]. Frontiers in medicine, 2026 doi:10.3389/fmed.2026.1801630.
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