Effect of Tricin on cardiomyocyte damage caused by diabetic cardiomyopathy (DCM)

2024

BMC Cardiovascular Disorders, Vol 24, Iss 1, Pp 1-8 (2024)

Abstract 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.

article

English

BMC, 2024.

Tricin, Diabetic cardiomyopathy, Oxidative stress, Inflammatory, TLR4/MyD88/NF-κB signaling pathway, Diseases of the circulatory (Cardiovascular) system, RC666-701