Pathology, research and practice · 2026
Curcumin nanoparticles attenuate sepsis-induced myocardial injury by modulating the Nrf2/HO-1/SLC7A11/GPX4 and ACSL4/LPCAT3 pathways.
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Wang Yuhang, Zhang Han, Liu Jiaqi, Lin Rimei, Huang Yingyu, Liu Xinrui, Dong Yunqi, Lu Hongkui, Wei Yutong, Lv Haoze, Liu Xinyu, Sun Cong
Аннотация
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.
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.