Exploring the potential of kinsenoside as a functional food bioactive: attenuation of isoproterenol-induced H9c2 cell damage through NLRP3 inflammasome inhibition
Main Article Content
Keywords
cardiomyocyte hypertrophy, heart failure, kinsenoside, NLRP3 inflammasome, oxidative stress
Abstract
This study examines the protective effects of Kinsenoside (KD), a natural bioactive compound, against inflammation, oxidative stress, and cardiomyocyte hypertrophy in isoproterenol (ISO)-stimulated H9c2 cells, which serve as an in vitro model of heart failure (HF). The effects of KD were assessed using various assays, including the CCK-8 assay for cell viability, LDH detection for cell membrane integrity, qPCR for gene expression, ELISA for inflammatory cytokine quantification, and immunostaining for hypertrophy assessment. KD significantly enhanced the viability of ISO-stimulated H9c2 cells (p < 0.05) and reduced ISO-induced production of inflammatory cytokines, such as IL-6, IL-1β, and TNF-α (p < 0.05). Furthermore, KD reduced oxidative stress markers (p < 0.05) and alleviated cardiomyocyte hypertrophy induced by ISO stimulation (p < 0.05). Mechanistically, KD inhibited NLRP3 inflammasome activation (p < 0.05), a critical mediator of inflammation and cellular damage in this model. These results suggest that KD protects H9c2 cells from isoproterenol-induced injury by suppressing NLRP3 inflammasome activation. Due to its natural bioactive properties, KD may serve as a potential therapeutic agent for mitigating HF progression and as a functional food ingredient for cardiovascular health support.
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