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Background Shenfu injection (SFI), derived from a traditional Chinese medicine (TCM) prescription, is an effective drug for the treatment of sepsis-induced myocardial injury (SIMI) with good efficacy, but its exact therapeutic mechanism remains unclear. Methods SwissTargetPrediction and GeneCards database were used to obtain relevant targets for SFI and SIMI. STRING 11.5 and MCODE were used to analyse potential therapeutic targets for SFI. DAVID 6.8 database was used to perform enrichment analysis. In addition, the SIMI model was constructed by cecal ligation and puncture (CLP) on Sprague Dawley rats and the related protein expression levels were verified by AutoDock Vina 1.1.2 and experiment. Results SFI has a total of 10 main active compounds and treats SIMI through 52 potential targets, among which LGALS3, STAT3, FGF1, and AKT1 were the core targets for treatment. Based on enrichment analysis, STAT3, FGF1, and AKT1 in the core targets were experimentally validated. The experimental results showed that SFI effectively ameliorated the inflammatory response and myocardial injury and inhibited apoptosis in SIMI. And SFI improved SIMI by decreasing caspase-9, STAT3 and phospho-AKT1 (p-AKT1) expression, and enhancing FGF1 expressions. Conclusions This study showed that SFI effectively reduced the expression of caspase-9, STAT3 and p-AKT1, enhanced the expression of FGF1, reduced the inflammatory response, inhibited apoptosis and attenuated cardiac injury to SIMI.背景 参附注射液（Shenfu injection, SFI）源自中药方剂，是治疗脓毒症诱导心肌损伤（sepsis-induced myocardial injury, SIMI）的有效药物，临床疗效良好，但其确切的治疗机制仍未明确。 方法 本研究采用SwissTargetPrediction与GeneCards数据库获取参附注射液与脓毒症诱导心肌损伤的相关靶点；使用STRING 11.5与MCODE分析参附注射液的潜在治疗靶点；借助DAVID 6.8数据库开展富集分析。此外，通过盲肠结扎穿刺（cecal ligation and puncture, CLP）法构建斯普拉格-道利（Sprague Dawley）大鼠脓毒症诱导心肌损伤模型，并采用AutoDock Vina 1.1.2结合实验验证相关蛋白的表达水平。 结果 参附注射液共含10种主要活性成分，通过52个潜在靶点发挥治疗脓毒症诱导心肌损伤的作用，其中LGALS3、STAT3、FGF1及AKT1为核心治疗靶点。基于富集分析结果，核心靶点中的STAT3、FGF1与AKT1均经实验验证。实验结果显示，参附注射液可有效改善脓毒症诱导心肌损伤的炎症反应与心肌损伤，并抑制细胞凋亡；其通过下调caspase-9、STAT3及磷酸化AKT1（phospho-AKT1, p-AKT1）的表达，上调FGF1的表达，从而改善脓毒症诱导心肌损伤。 结论 本研究证实，参附注射液可有效下调caspase-9、STAT3及p-AKT1的表达，上调FGF1的表达，减轻炎症反应、抑制细胞凋亡并缓解脓毒症诱导心肌损伤。