Phytomedicine : international journal of phytotherapy and phytopharmacology · 2026
Lycorine improves inflammatory imbalance in diabetic cardiomyopathy by targeting ILF3.
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Zhou Qian, Jin Xuejin, Yuan Miao, Tao Huanyan, Bao Shenjie, Zhang Jingnan, Xu Zheng, Chattipakorn Nipon, Wang Yi, Zhu Hong, Liang Guang
Аннотация
BACKGROUND: Diabetic cardiomyopathy (DCM) is characterized by chronic low-grade inflammation and metabolic disturbances, leading to progressive cardiac dysfunction. Lycorine (LY), a complex tetracyclic pyrrolo[de]phenanthridine alkaloid from the Amaryllidaceae family, has shown potential anti-inflammatory effects, but its role in DCM pathogenesis remains unexplored.
PURPOSE: This study investigated the cardioprotective effect of LY in DCM and its underlying molecular mechanisms.
METHODS: We employed both in vitro (high glucose/palmitic acid-treated cardiomyocytes) and in vivo (streptozotocin-induced diabetic mice) models to investigate LY's cardioprotective effects. Liquid chromatography-tandem mass spectrometry, molecular docking, surface plasmon resonance binding assay, cellular thermal shift assay, and RNA interference approaches were utilized to identify the key target and mechanistic pathways.
RESULTS: In vitro and in vivo models of DCM revealed that LY significantly attenuated cardiac inflammation. Mechanistically, liquid chromatography-tandem mass spectrometry analysis revealed that LY targeted interleukin enhancer-binding factor 3 (ILF3), a critical regulator of inflammatory responses. Notably, surface plasmon resonance and cellular thermal shift assay data validated a direct interaction between LY and ILF3. By interacting with ILF3, LY enhanced nuclear factor erythroid 2-related factor 2-mediated anti-inflammatory responses while suppressing NF-κB-driven pro-inflammatory signaling, thereby restoring inflammatory homeostasis and reducing myocardial injury. Furthermore, ILF3 knockdown mimicked the protective effects of LY, and ILF3 activity was essential for LY's cardioprotective effects.
CONCLUSION: These findings suggest that LY ameliorates DCM by modulating ILF3-dependent nuclear factor erythroid 2-related factor 2 and NF-κB crosstalk to restore inflammatory balance, suggesting its potential as a novel therapeutic agent for diabetic cardiovascular complications.
PURPOSE: This study investigated the cardioprotective effect of LY in DCM and its underlying molecular mechanisms.
METHODS: We employed both in vitro (high glucose/palmitic acid-treated cardiomyocytes) and in vivo (streptozotocin-induced diabetic mice) models to investigate LY's cardioprotective effects. Liquid chromatography-tandem mass spectrometry, molecular docking, surface plasmon resonance binding assay, cellular thermal shift assay, and RNA interference approaches were utilized to identify the key target and mechanistic pathways.
RESULTS: In vitro and in vivo models of DCM revealed that LY significantly attenuated cardiac inflammation. Mechanistically, liquid chromatography-tandem mass spectrometry analysis revealed that LY targeted interleukin enhancer-binding factor 3 (ILF3), a critical regulator of inflammatory responses. Notably, surface plasmon resonance and cellular thermal shift assay data validated a direct interaction between LY and ILF3. By interacting with ILF3, LY enhanced nuclear factor erythroid 2-related factor 2-mediated anti-inflammatory responses while suppressing NF-κB-driven pro-inflammatory signaling, thereby restoring inflammatory homeostasis and reducing myocardial injury. Furthermore, ILF3 knockdown mimicked the protective effects of LY, and ILF3 activity was essential for LY's cardioprotective effects.
CONCLUSION: These findings suggest that LY ameliorates DCM by modulating ILF3-dependent nuclear factor erythroid 2-related factor 2 and NF-κB crosstalk to restore inflammatory balance, suggesting its potential as a novel therapeutic agent for diabetic cardiovascular complications.