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Updated: Jun 29, 2025

Herbal Munziq Ameliorates Myocardial Ischemia-Reperfusion Injury by Inhibiting Inflammation
Published on: January 10, 2025
Nuciferine reduces vascular leakage and improves cardiac function in acute myocardial infarction by regulating the
Wei Xie1,2, Shumin Chen3, Wenzhe Wang1,2
1Department of Cardio-Thoracic Surgery, Nanjing Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medical School, Nanjing, 210008, Jiangsu, China.
Insights
Nuciferine protects against acute myocardial infarction (AMI) by preserving microvascular integrity and cardiac function. It achieves this by strengthening endothelial cell barriers and activating the PI3K/AKT pathway, crucial for cardiovascular health.
Area of Science:
- Cardiovascular Research
- Pharmacology
- Cell Biology
Background:
- Microvascular damage significantly impacts patient outcomes in acute myocardial infarction (AMI).
- Nuciferine shows potential for cardiovascular disease treatment, but its role in AMI-related microvascular injury is not well understood.
Purpose of the Study:
- To investigate the protective effects of nuciferine on microvascular structure and function during AMI.
- To elucidate the underlying mechanisms of nuciferine's action, focusing on the PI3K/AKT pathway.
Main Methods:
- In vivo studies assessed cardiac function and pathology in an AMI model treated with nuciferine.
- In vitro experiments evaluated nuciferine's effects on human coronary microvascular endothelial cells (HCMECs) under oxygen-glucose deprivation (OGD).
- Analysis included endothelial cell permeability, adherens junctions, and PI3K/AKT pathway phosphorylation, with and without PI3K inhibitors like wortmannin.
Main Results:
- Nuciferine treatment improved cardiac function, reduced cardiomyocyte damage, and inhibited vascular leakage in vivo.
- In vitro, nuciferine protected HCMECs from OGD-induced injury, preserving structure and function.
- Nuciferine significantly increased PI3K/AKT pathway phosphorylation, an effect reversed by wortmannin.
Conclusions:
- Nuciferine demonstrates a protective effect against AMI-induced microvascular injury.
- The mechanism involves the regulation of the PI3K/AKT pathway and enhancement of endothelial barrier function.
- Nuciferine holds promise for therapeutic intervention in acute myocardial infarction by safeguarding microvascular integrity.
Abstract:
The destruction of the microvascular structure and function can seriously affect the survival and prognosis of patients with acute myocardial infarction (AMI). Nuciferine has a potentially beneficial effect in the treatment of cardiovascular disease, albeit its role in microvascular structure and function during AMI remains unclear. This study aimed to investigate the protective effect and the related mechanisms of nuciferine in microvascular injury during AMI. Cardiac functions and pathological examination were conducted in vivo to investigate the effect of nuciferine on AMI. The effect of nuciferine on permeability and adherens junctions in endothelial cells was evaluated in vitro, and the phosphorylation level of the PI3K/AKT pathway (in the presence or absence of PI3K inhibitors) was also analyzed. In vivo results indicated that nuciferine inhibited ischemia-induced cardiomyocyte damage and vascular leakage and improved cardiac function. In addition, the in vitro results revealed that nuciferine could effectively inhibit oxygen-glucose deprivation (OGD) stimulated breakdown of the structure and function of human coronary microvascular endothelial cells (HCMECs). Moreover, nuciferine could significantly increase the phosphorylation level of the PI3K/AKT pathway. Finally, the inhibitor wortmannin could reverse the protective effect of nuciferine on HCMECs. Nuciferine inhibited AMI-induced microvascular injury by regulating the PI3K/AKT pathway and protecting the endothelial barrier function in mice.
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