Key result
Tricin significantly ameliorated high glucose-induced oxidative stress and suppressed pro-inflammatory cytokines and the TLR4-MYD88-NF-κB signaling pathway in a dose-dependent manner.
Why the study?
The specific mechanisms by which Tricin exerts its effects in diabetic cardiomyopathy remained to be elucidated.
Does Tricin reduce oxidative stress and inflammation in a high glucose-induced diabetic cardiomyopathy cell model?
Does Tricin reduce oxidative stress and inflammation in a high glucose-induced diabetic cardiomyopathy cell model?
p-value: p=<0.05
Tricin exhibits a protective role against high glucose-induced cardiac damage in vitro by reducing oxidative stress and inflammation via inhibition of the TLR4-MYD88-NF-κB pathway.
Tricin may protect against high-glucose cardiac injury in vitro; leaves open translation to in vivo or clinical diabetic cardiomyopathy.
OBJECTIVES: Flavonoid compounds exhibit remarkable antioxidant and anti-inflammatory properties in DCM and various other diseases. However, the specific mechanisms by which Tricin, 4',5,7-trihydroxy-3',5'-dimethoxyflavone, exerts its effects in the context of DCM remain to be elucidated. METHODS: Rat H9C2 cells were cultured and subjected to high glucose conditions to establish a DCM cell model. Tricin was administered in varying concentrations to evaluate its effects on cellular oxidative stress markers, including ROS, LDH, and SOD. Additionally, the levels of inflammatory cytokines TNF-α, IL-1β, and IL-6, as well as the expression of TLR4, MYD88, and p-NF-κB, were assessed through ELISA and Western blotting. RESULTS: Tricin treatment significantly ameliorated high glucose-induced oxidative stress in H9C2 cells, evidenced by reduced ROS and LDH levels and increased SOD levels in a dose-dependent manner. Furthermore, Tricin effectively suppressed the elevation of pro-inflammatory cytokines TNF-α, IL-1β, and IL-6. Tricin also inhibited the overactivation of the TLR4-MYD88-NF-κB signaling pathway, suggesting its role in modulating key inflammatory processes in DCM. CONCLUSIONS: Tricin exhibits a protective role against high glucose-induced cardiac damage in a DCM cell model. By reducing oxidative stress and inflammation, and inhibiting the TLR4-MYD88-NF-κB pathway, Tricin shows significant therapeutic potential for DCM treatment. This study underscores the value of Tricin as a novel therapeutic approach for managing diabetic cardiomyopathy, warranting further research and clinical investigation. CLINICAL TRIAL NUMBER: Not applicable.
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Yu et al. (2024) studied Diabetic cardiomyopathy (DCM). Tricin vs. High glucose (150 mM) without Tricin was evaluated on Oxidative stress markers (ROS, LDH, SOD) and inflammatory cytokines (TNF-α, IL-1β, IL-6) (p=<0.05). Tricin significantly ameliorated high glucose-induced oxidative stress and suppressed pro-inflammatory cytokines and the TLR4-MYD88-NF-κB signaling pathway in a dose-dependent manner.
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