Sulforaphane prevents angiotensin II-induced cardiomyopathy by activation of Nrf2 via stimulating the Akt/GSK-3ß/Fyn pathway

摘要: Abstract Aims Activation of nuclear factor erythroid 2-related 2 (Nrf2) by sulforaphane (SFN) protects from, and deletion the Nrf2 gene exaggerates, diabetic cardiomyopathy. Angiotensin II (Ang II) plays a critical role in development Therefore, whether SFN prevents Ang II-induced cardiomyopathy through activation was examined using wild-type, global (Nrf2-KO) cardiomyocyte-specific overexpression (Nrf2-TG) mice. Methods results Administration subpressor dose to wild-type mice induced cardiac oxidative stress, inflammation, remodeling dysfunction, all which could be prevented treatment with up-regulation activation. Nrf2-KO are susceptible, Nrf2-TG resistant, respectively, Meanwhile, ability protect against damage lost Up-regulation is accompanied Akt, inhibition glycogen synthase kinase (GSK)-3β, accumulation Fyn nuclei. In vitro abolished increased when cells were exposed PI3K inhibitor or GSK-3β-specific activator. Conclusion These suggest that central prevention cardiomyopathy, partially via Akt/GSK-3β/Fyn-mediated