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.
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.