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<p>Yixinshu (YXS), a traditional Chinese formula, is applied for coronary artery diseases in clinic, however, its cardioprotective mechanisms remain unclear. At present, the role and underlying mechanisms of YXS is to elucidate in enhancing post-myocardial infarction (MI) recovery. MI mouse models and hypoxia-injured cardiomyocytes were reproduced to evaluate YXS efficacy. The pharmacological targets and blood-absorbed compounds of YXS were determined by network pharmacology and LC–MS, respectively. Bioactive components were screened via molecular docking and surface plasmon resonance (SPR), and mechanisms were validated by molecular assays. YXS improved cardiac function and reduced infarct size. These effects were linked to preserved mitochondrial homeostasis and reduced apoptosis through the SHP1/JAK2/STAT3 pathway. Dihydrotanshinone Ⅰ (DHT), a key compound identified in plasma, suppressed SHP1, activated STAT3, and mitigated mitochondrial injury. SHP1 overexpression could abolish DHT’s protection effects. Taken together, YXS could exert cardioprotection in MI by modulating mitochondrial function and apoptosis via the SHP1/JAK2/STAT3 axis, and DHT is potential beneficial bioactive ingredient mediating these effects.</p>

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Yixinshu attenuates myocardial infarction via SHP1/JAK2/STAT3-mediated regulation of mitochondrial function and apoptosis

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年3月4日

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  • Xueting Wang,
  • Xinrui Wang,
  • Yang Liu,
  • Yang Cui,
  • Keyi Chen,
  • Hongkun Wu,
  • Mingshan Zhang,
  • Ming Liao,
  • Linyun Fu,
  • Xiangchun Shen

摘要

Yixinshu (YXS), a traditional Chinese formula, is applied for coronary artery diseases in clinic, however, its cardioprotective mechanisms remain unclear. At present, the role and underlying mechanisms of YXS is to elucidate in enhancing post-myocardial infarction (MI) recovery. MI mouse models and hypoxia-injured cardiomyocytes were reproduced to evaluate YXS efficacy. The pharmacological targets and blood-absorbed compounds of YXS were determined by network pharmacology and LC–MS, respectively. Bioactive components were screened via molecular docking and surface plasmon resonance (SPR), and mechanisms were validated by molecular assays. YXS improved cardiac function and reduced infarct size. These effects were linked to preserved mitochondrial homeostasis and reduced apoptosis through the SHP1/JAK2/STAT3 pathway. Dihydrotanshinone Ⅰ (DHT), a key compound identified in plasma, suppressed SHP1, activated STAT3, and mitigated mitochondrial injury. SHP1 overexpression could abolish DHT’s protection effects. Taken together, YXS could exert cardioprotection in MI by modulating mitochondrial function and apoptosis via the SHP1/JAK2/STAT3 axis, and DHT is potential beneficial bioactive ingredient mediating these effects.