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

Publisher: BioMed Central Country of Publication: England NLM ID: 100968539 Publication Model: Electronic Cited Medium: Internet ISSN: 1471-2261 (Electronic) Linking ISSN: 14712261 NLM ISO Abbreviation: BMC Cardiovasc Disord Subsets: MEDLINE

Original Publication: London : BioMed Central, [2001-

Myocytes, Cardiac*/drug effects ; Myocytes, Cardiac*/pathology ; Myocytes, Cardiac*/metabolism ; Oxidative Stress*/drug effects ; Diabetic Cardiomyopathies*/metabolism ; Diabetic Cardiomyopathies*/drug therapy ; Diabetic Cardiomyopathies*/pathology ; Diabetic Cardiomyopathies*/etiology ; Toll-Like Receptor 4*/metabolism ; Signal Transduction*/drug effects ; Myeloid Differentiation Factor 88*/metabolism ; Antioxidants*/pharmacology ; Inflammation Mediators*/metabolism ; NF-kappa B*/metabolism ; Reactive Oxygen Species*/metabolism ; Anti-Inflammatory Agents*/pharmacology ; Cytokines*/metabolism; Animals ; Rats ; Cell Line ; Glucose/metabolism ; Glucose/toxicity ; Flavonoids/pharmacology ; Dose-Response Relationship, Drug

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.
Competing Interests: Declarations. Ethics approval and consent to participate: Not applicable. Competing interests: The authors declare no competing interests.
(© 2024. The Author(s).)

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2023ZYYC2040 Shanxi Province Traditional Chinese Medicine Research Topic

Keywords: Diabetic cardiomyopathy; Inflammatory; Oxidative stress; TLR4/MyD88/NF-κB signaling pathway; Tricin

0 (Toll-Like Receptor 4)
0 (Myeloid Differentiation Factor 88)
0 (Tlr4 protein, rat)
0 (Antioxidants)
0 (Inflammation Mediators)
0 (NF-kappa B)
0 (Reactive Oxygen Species)
0 (Anti-Inflammatory Agents)
0 (Myd88 protein, rat)
0 (Cytokines)
IY9XDZ35W2 (Glucose)
0 (Flavonoids)

Date Created: 20241123 Date Completed: 20241123 Latest Revision: 20241125

20241126

PMC11585224

10.1186/s12872-024-04295-y

39578745