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Objective <p>To investigate the underlying mechanism of Ling-Gui-Zhu-Gan Decoction (LGZGD) in reducing hyperinflammatory responses to provide cardioprotective effects.</p> Methods <p>The main chemical components of LGZGD were identified using ultra-high performance liquid chromatography. <i>In vivo</i>, the rats were randomly divided into 4 groups using simple randomization: the sham group, the model group, the LGZGD (4.2 g/kg) group, and captopril (4.375 mg/kg) group, 6 in each group. A rat model of ventricular remodeling (VR) after acute myocardial infarction (AMI) was established by ligation of the left anterior descending coronary artery. After 4 weeks of treatment, cardiac function was evaluated by echocardiography, and histopathological changes were examined using HE and Masson stainings. Serum levels of cardiac enzymes and oxidative stress markers were measured with microplate assays. Reactive oxygen species (ROS) were visualized by fluorescence staining, while protein and mRNA levels were analyzed by Western blot and RT-qPCR. Levels of proinflammatory cytokines and trimethylamine N-oxide (TMAO) were quantified through ELISA. <i>In vitro</i>, H9c2 cells were exposed to 400 µmol/L TMAO, and oxidative stress markers were measured by microplate assay. ROS levels were visualized using fluorescence staining, and gene and protein expression were analyzed by RT-PCR and Western blot. Proinflammatory cytokines and TMAO levels were further evaluated by ELISA.</p> Results <p>LGZGD was found to contain liquiritin, isoliquiritin, coumarin, liquiritigenin, cinnamic acid, kaempferol, cinnamaldehyde, glycyrrhizic acid, and atractylenolide III. <i>In vivo</i>, LGZGD improved cardiac function, reduced myocardial pathology, lowered serum cardiac enzymes and TMAO, decreased oxidative stress, regulated the expression of genes and proteins within the ROS/thioredoxin-interacting protein (TXNIP)/NACHT, LRR, and PYD domains-containing protein 3 (NLRP3) pathway, and suppressed the secretion of IL-1β and IL-18 (<i>P</i>&lt;0.01). <i>In vitro</i> analysis showed that LGZGD significantly decreased markers of myocardial injury, alleviated oxidative stress, and inhibited the secretion of IL-1β and IL-18 in TMAO-stimulated H9c2 cells (<i>P</i>&lt;0.01).</p> Conclusion <p>LGZGD ameliorates TMAO-induced myocardial injury by modulating the ROS/TXNIP/NLRP3 signaling pathway.</p>

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Cardioprotective Effects of Ling-Gui-Zhu-Gan Decoction Against Ventricular Remodeling after Acute Myocardial Infarction via ROS/TXNIP/NLRP3 Signaling

  • 期刊论文

  • 发表日期：

    2026年3月7日

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  • Yao-yao Ma,
  • Lu-qin Guo,
  • Lan Zhou,
  • Xiao-ni Zhao,
  • Shu-shu Wang,
  • Liang Wang,
  • Jin-ling Huang,
  • Peng Zhou

摘要

Objective

To investigate the underlying mechanism of Ling-Gui-Zhu-Gan Decoction (LGZGD) in reducing hyperinflammatory responses to provide cardioprotective effects.

Methods

The main chemical components of LGZGD were identified using ultra-high performance liquid chromatography. In vivo, the rats were randomly divided into 4 groups using simple randomization: the sham group, the model group, the LGZGD (4.2 g/kg) group, and captopril (4.375 mg/kg) group, 6 in each group. A rat model of ventricular remodeling (VR) after acute myocardial infarction (AMI) was established by ligation of the left anterior descending coronary artery. After 4 weeks of treatment, cardiac function was evaluated by echocardiography, and histopathological changes were examined using HE and Masson stainings. Serum levels of cardiac enzymes and oxidative stress markers were measured with microplate assays. Reactive oxygen species (ROS) were visualized by fluorescence staining, while protein and mRNA levels were analyzed by Western blot and RT-qPCR. Levels of proinflammatory cytokines and trimethylamine N-oxide (TMAO) were quantified through ELISA. In vitro, H9c2 cells were exposed to 400 µmol/L TMAO, and oxidative stress markers were measured by microplate assay. ROS levels were visualized using fluorescence staining, and gene and protein expression were analyzed by RT-PCR and Western blot. Proinflammatory cytokines and TMAO levels were further evaluated by ELISA.

Results

LGZGD was found to contain liquiritin, isoliquiritin, coumarin, liquiritigenin, cinnamic acid, kaempferol, cinnamaldehyde, glycyrrhizic acid, and atractylenolide III. In vivo, LGZGD improved cardiac function, reduced myocardial pathology, lowered serum cardiac enzymes and TMAO, decreased oxidative stress, regulated the expression of genes and proteins within the ROS/thioredoxin-interacting protein (TXNIP)/NACHT, LRR, and PYD domains-containing protein 3 (NLRP3) pathway, and suppressed the secretion of IL-1β and IL-18 (P<0.01). In vitro analysis showed that LGZGD significantly decreased markers of myocardial injury, alleviated oxidative stress, and inhibited the secretion of IL-1β and IL-18 in TMAO-stimulated H9c2 cells (P<0.01).

Conclusion

LGZGD ameliorates TMAO-induced myocardial injury by modulating the ROS/TXNIP/NLRP3 signaling pathway.