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Войти в исследования Phytomedicine : international journal of phytotherapy and phytopharmacology · 2025
Houttuynia cordata-derived nanoparticles stabilize mitochondrial dynamics to alleviate ulcerative colitis via the Nrf2/Ho-1 pathways.
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Zhuang Wenyi, Qu Mengqi, Guan Yang, Pan Jieli, Tai Yan, Xie Guanqun, Chen Xiaohui, Zhu Feiye
Аннотация
BACKGROUND: Ulcerative colitis (UC), a chronic inflammatory bowel disease, faces limited treatment efficacy and safety concerns. Extracellular vesicles (EVs) offer a promising nanoplatform for targeted therapy.
PURPOSE: This study aimed to isolate and characterize houttuynia cordata-derived nanoparticles (HDNPs) and evaluate their therapeutic potential in UC by targeting dual pathological axes: mitochondrial dynamics dysregulation and oxidative-inflammatory cascades, aiming to address unmet needs in current UC therapies.
METHODS: In vitro studies using LPS-stimulated Caco-2 cells (modeling inflamed intestinal epithelia) to evaluate mitochondrial dynamics, Nrf2/Ho-1 activation, oxidative stress. In vivo validation was performed in a DSS-induced murine UC model, assessing clinical parameters, histopathology and molecular markers.
RESULTS: HDNPs administration significantly attenuated DSS-induced weight loss and elevated disease activity index, while preserving intestinal mucosal integrity. In vitro, HDNPs markedly reduced intracellular oxidative markers, activated Nrf2 signaling, and upregulated Ho-1 synthesis. Notably, Nrf2 inhibition abolished HDNPs' protective effects, confirming the critical role of this pathway in mediating therapeutic outcomes.
CONCLUSION: HDNPs stabilize mitochondrial dynamics to restore epithelial energy homeostasis and activating the Nrf2/Ho-1 axis to suppress oxidative-inflammatory cascades, addressing critical limitations of conventional UC therapies and offering translational potential for clinical application.
PURPOSE: This study aimed to isolate and characterize houttuynia cordata-derived nanoparticles (HDNPs) and evaluate their therapeutic potential in UC by targeting dual pathological axes: mitochondrial dynamics dysregulation and oxidative-inflammatory cascades, aiming to address unmet needs in current UC therapies.
METHODS: In vitro studies using LPS-stimulated Caco-2 cells (modeling inflamed intestinal epithelia) to evaluate mitochondrial dynamics, Nrf2/Ho-1 activation, oxidative stress. In vivo validation was performed in a DSS-induced murine UC model, assessing clinical parameters, histopathology and molecular markers.
RESULTS: HDNPs administration significantly attenuated DSS-induced weight loss and elevated disease activity index, while preserving intestinal mucosal integrity. In vitro, HDNPs markedly reduced intracellular oxidative markers, activated Nrf2 signaling, and upregulated Ho-1 synthesis. Notably, Nrf2 inhibition abolished HDNPs' protective effects, confirming the critical role of this pathway in mediating therapeutic outcomes.
CONCLUSION: HDNPs stabilize mitochondrial dynamics to restore epithelial energy homeostasis and activating the Nrf2/Ho-1 axis to suppress oxidative-inflammatory cascades, addressing critical limitations of conventional UC therapies and offering translational potential for clinical application.