Hossain Nusrat, Shabnam Sadia, Emran Tushar, Zahid Zahidul Islam, Alam Shaiful, Bepari Asim Kumar, Sayedur Rahman G M, Reza Hasan Mahmud
Department of Pharmaceutical Sciences, North South University, Dhaka, 1229, Bangladesh.
Department of Pharmaceutical Sciences, North South University, Dhaka, 1229, Bangladesh.
Arch Biochem Biophys. 2025 Jul;769:110444. doi: 10.1016/j.abb.2025.110444. Epub 2025 Apr 28.
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 (CoQ) in reducing oxidative stress due to its antioxidant properties. However, the cardioprotective and nephroprotective roles of CoQ against the toxicity induced by fludrocortisone acetate (FCA) have yet to be investigated. Therefore, we evaluated the CoQ 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 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 in these rats. Histopathological examination detected tissue damage and fibrosis in the FCA-Salt group, which was significantly reduced by CoQ. Furthermore, enzyme-linked immunosorbent assay (ELISA) indicated the activation of Transforming growth factor-β1/Tumor necrosis factor-α (TGF-β1/TNF-α) by CoQ. Consequently, our study suggests that CoQ can effectively protect heart and kidney health against cardiotoxicity and nephrotoxicity in FCA-Salt hypertensive rats via TGF-β1/TNF-α pathway.
高血压是导致心脏重塑的最常见因素之一，而心脏重塑与心脏和肾脏功能的变化相关。多项研究报道了辅酶Q（CoQ）因其抗氧化特性在减轻氧化应激方面的有益作用。然而，CoQ对醋酸氟氢可的松（FCA）诱导的毒性的心脏保护和肾脏保护作用尚未得到研究。因此，我们在大鼠模型（FCA-盐模型）中评估了CoQ对FCA诱导的心脏毒性和肾脏毒性的影响。我们使用生化分析方法分析了各种氧化应激参数和抗氧化酶活性。此外，我们通过对心脏和肾脏组织进行组织学染色来检测炎症和纤维化情况。在FCA-盐模型大鼠中，CoQ显著降低了脂质过氧化产物丙二醛（MDA），同时增加了一氧化氮（NO）。CoQ还增强了这些大鼠的抗氧化酶活性。组织病理学检查发现FCA-盐模型组存在组织损伤和纤维化，而CoQ使其显著减轻。此外，酶联免疫吸附测定（ELISA）表明CoQ激活了转化生长因子-β1/肿瘤坏死因子-α（TGF-β1/TNF-α）。因此，我们的研究表明，CoQ可以通过TGF-β1/TNF-α途径有效保护FCA-盐模型高血压大鼠的心脏和肾脏健康，使其免受心脏毒性和肾脏毒性的影响。
