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Updated: Feb 2, 2026

Herbal Munziq Ameliorates Myocardial Ischemia-Reperfusion Injury by Inhibiting Inflammation
Published on: January 10, 2025
Curcumin nanoparticles attenuate sepsis-induced myocardial injury by modulating the Nrf2/HO-1/SLC7A11/GPX4 and
Yuhang Wang1, Han Zhang1, Jiaqi Liu1
1College of Pharmacy, Changchun University of Chinese Medicine, Changchun 130117, China.
Background And Objectives:
Sepsis-Induced Myocardial Injury (SIMI) poses a serious threat to patients' lives. Although curcumin (Cur) has potential therapeutic effects on SIMI, its clinical application is hindered by the limitation of low bioavailability. The emergence of nanodelivery systems provides novel strategies to address this issue. This study aimed to investigate the therapeutic effects of curcumin nanoparticles (Cur-NPs) on septic myocarditis (SIMI) and its potential molecular mechanisms.
Materials And Methods:
Cur-NPs were prepared using the ion cross-linking method, and a septicemia mouse model was established by intraperitoneal injection of lipopolysaccharide (LPS). Immunofluorescence, Western blot (WB), real-time quantitative PCR (RT-qPCR), and other molecular biology techniques were employed to systematically explore the molecular mechanisms underlying the therapeutic effects of Cur-NPs on SIMI.
Results:
Cur-NPs significantly alleviated myocardial tissue damage induced by septicemia and effectively mitigated inflammatory responses and mitochondrial damage. Mechanistic studies revealed that Cur-NPs upregulated the expression levels of Nuclear Factor Erythroid 2-Related Factor 2 (Nrf2), Heme Oxygenase-1 (HO-1), Solute Carrier Family 7 Member 11 (SLC7A11), Glutathione Peroxidase 4 (GPX4), Ferroptosis-suppressor-protein 1 (FSP1), and ferritin, while downregulating the expression of Acyl-CoA Synthetase Long Chain Family Member 4 (ACSL4), LysoPHosPHatidylcholine Acyltransferase 3 (LPCAT3), and 4-hydroxynonenal (4-HNE), thereby inhibiting ferroptosis in cardiomyocytes.
Conclusions:
Cur-NPs can effectively alleviate SIMI by dual regulation of the Nrf2/HO-1/xCT/GPX4 pathway and the ACSL4/LPCAT3 pathway, providing a promising new approach for the clinical treatment of SIMI.
Insights
Curcumin nanoparticles effectively treat sepsis-induced myocardial injury by inhibiting ferroptosis. This novel nanodelivery system improves curcumin
Area of Science:
- Cardiovascular Research
- Nanomedicine
- Molecular Biology
Background:
- Sepsis-induced myocardial injury (SIMI) is a life-threatening condition.
- Curcumin (Cur) shows therapeutic potential for SIMI but suffers from low bioavailability.
- Nanodelivery systems offer a strategy to enhance curcumin's efficacy.
Purpose of the Study:
- To investigate the therapeutic effects of curcumin nanoparticles (Cur-NPs) on SIMI.
- To elucidate the molecular mechanisms underlying Cur-NPs' action in septic myocarditis.
Main Methods:
- Cur-NPs were prepared using ion cross-linking.
- A mouse model of septicemia was induced by lipopolysaccharide (LPS).
- Molecular biology techniques including immunofluorescence, Western blot, and RT-qPCR were used.
Main Results:
- Cur-NPs significantly reduced myocardial damage, inflammation, and mitochondrial injury in septic mice.
- Cur-NPs modulated key proteins involved in ferroptosis, including upregulation of Nrf2, HO-1, SLC7A11, GPX4, FSP1, and ferritin.
- Cur-NPs downregulated ferroptosis markers ACSL4, LPCAT3, and 4-HNE.
Conclusions:
- Cur-NPs effectively alleviate SIMI by inhibiting ferroptosis in cardiomyocytes.
- Therapeutic effects are mediated by dual regulation of the Nrf2/HO-1/xCT/GPX4 and ACSL4/LPCAT3 pathways.
- Cur-NPs represent a promising therapeutic strategy for clinical treatment of SIMI.
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