Coenzyme Q10 alleviates oxidative stress, inflammation and fibrosis via activation of TGFβ1/TNF-α in FCA-Salt hypertensive rats

Hypertension is one of the most common factors contributing to cardiac remodeling that links to changes in both heart and kidney functions. Several studies have reported the beneficial effects of Coenzyme Q 10 (CoQ 10 ) in reducing oxidative stress due to its antioxidant properties. However, the cardioprotective and nephroprotective roles of CoQ 10 against the toxicity induced by fludrocortisone acetate (FCA) have yet to be investigated. Therefore, we evaluated the CoQ 10 effects on FCA-induced cardiotoxicity and nephrotoxicity in a rat model (FCA-Salt). We analyzed various oxidative stress parameters and antioxidant enzyme activities using biochemical assays. In addition, we examined inflammatory and fibrosis via histological staining of heart and kidney tissues. CoQ 10 significantly reduced lipid peroxidation product-malondialdehyde (MDA) while increased nitric oxide (NO) in the FCA-Salt rats. Antioxidant enzyme activities were also enhanced by CoQ 10 in these rats. Histopathological examination detected tissue damage and fibrosis in the FCA-Salt group, which was significantly reduced by CoQ 10 . Furthermore, enzyme-linked immunosorbent assay (ELISA) indicated the activation of Transforming growth factor-β1/Tumor necrosis factor-α (TGF-β1/TNF-α) by CoQ 10 . Consequently, our study suggests that CoQ 10 can effectively protect heart and kidney health against cardiotoxicity and nephrotoxicity in FCA-Salt hypertensive rats via TGF-β1/TNF-α pathway.