ArticleCardiovascular drugs and therapy2026
Paeoniflorin Alleviates Coronary Artery Lesions in Kawasaki Disease by Activating NRF2 Pathway and Inhibiting CYP2E1 Expression.
Article in Cardiovascular drugs and therapy, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- Protective Effects of Jiawei Baihu Tang in Kawasaki Disease: Omics Analysis and Mechanistic Exploration.Cardiovascular drugs and therapy · 2026Article
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Authors and funding
4 authors.
Funding
Abstract
purposeKawasaki disease (KD) is an acute systemic vasculitis causing coronary artery lesions (CAL). Paeoniflorin (PF) exerts anti-inflammatory and antioxidant properties, but its role in KD remains unclear. This study aims to elucidate the effects of PF on CAL and the underlying regulatory mechanisms.
methodsC57BL/6J mice were induced by Lactobacillus casei cell wall extract (LCWE) to establish a KD mouse model. Inflammatory infiltration and pathological changes of cardiac tissue in mice was evaluated by hematoxylin eosin staining. Oxidative damage of mice was evaluated by measuring protein carbonyl, 8-hydroxy-2'-deoxyguanosine, malondialdehyde and 4-hydroxynonenal (4-HNE). Superoxide dismutase, catalase, total antioxidant capacity and glutathione peroxidase 4 was measured to evaluate antioxidant levels in mice. Inflammation levels was assessed by measuring tumor necrosis factor-α (TNF-α), interleukin (IL)-1β and IL-6. Apoptosis of cardiac tissues was detected by TUNEL assay. The underlying mechanism was determined by RNA-sequencing.
resultsResults showed that PF inhibited inflammatory infiltration and apoptosis of cardiac tissues, as well as oxidative damage and inflammation in KD mouse model, but enhanced antioxidant levels in KD mouse model. Mechanically, PF inhibited cytochrome P450 family 2 subfamily E member 1 (CYP2E1) expression but activated NRF2 pathway in KD mouse model. CYP2E1 overexpression and ML385 (a NRF2 inhibitor) reversed the therapeutic effects of PF on KD mouse model. Moreover, CYP2E1 knockdown restored the therapeutic effects of PF inhibited by ML385 on KD mouse model.
conclusionCollectively, our findings demonstrated that PF alleviated CAL in KD by activating NRF2 pathway and inhibiting CYP2E1 expression. These results may provide a theoretical basis for the potential use of PF as a therapeutic agent for KD associated with CAL.
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Identifiers
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Registered trials
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