Attenuation of Cardiomyopathy Induced in Sub-Chronic Exposure of Acrolein by Sulforaphane via Indirect PPARy Expression Promoter

Abstract: Sulforaphane (SPN) is reported to activate the Nrf2/Keap1 complex responsible for protein and gene expression promotion of various antioxidant enzymes. The present study examined role Nrf2 in modulating other signaling pathways involved SPN’s attenuation acrolein (ACL)-induced cardiomyopathy rats. Forty-two rat was categorized into seven 4-week treatment groups: control, SPN, losartan (LTN), ACL, ACL+SPN, ACL+LTN, ACL+SPN+LTN. Heart samples were harvested analysis; cardiac oxidative injury biomarker levels histopathological examination undertaken. PPARγ, Nrf2, NF-κB, COX-2, CYP2E1 expressions examined. Results show that SPN SPN+LTN reduced GSH, catalase, lipid peroxidation compared ACL-treated group. Also, creatine kinase-MB, troponin, caspase 3 induced by ACL all attenuated. Altered tissue pathophysiology alleviated. significantly increased via PPARγ action but decreased NF-κB COX-2 expressions. ACLincreased attenuated combination. For first time, it suggests might offer a better therapeutic alternative ACL-induced activating reducing NF-κB/COX- 2/CYP2E1 Key words: Sulforaphane, Losartan, Acrolein, Cardiomyopathy, Oxidative Stress, PPARγ; Nrf2.