Protective role of scutellarin to counteract arsenic prompted renal damage in rats via the regulation of Nrf2/Keap1 pathway.

Arsenic intoxication is associated with acute renal failure which makes it a serious health concern worldwide. Scutellarin (SCU) is a flavonoid glucuronide that possesses a variety of therapeutic properties. Therefore, the current investigation was performed to ascertain the curative role of SCU to counteract arsenic instigated nephrotoxicity in rats. In this study, 48 albino rats were divided into four groups (n = 12/group): i) Control, ii) Arsenic (10 mgkg-1) group, iii) Arsenic + SCU (10 mgkg-1 +5 mgkg-1) treated group, and iv) SCU (5 mgkg-1) only treated group. Arsenic exposure downregulated the expressions of Nrf2, and its antioxidant genes, while increasing Keap-1 expressions. Arsenic administration reduced the activities of catalase (CAT), hemeoxygenase-1 (HO-1), superoxide dismutase (SOD), glutathione S-transferase (GST), glutathione (GSH), and glutathione peroxidase (GPx), whereas escalated malondialdehyde (MDA) and reactive oxygen species (ROS) contents. Arsenic treatment significantly elevated the levels of urea, creatinine, KIM-1 and NGAL, while reducing the level of creatinine clearance. Additionally, arsenic exposure elevated the levels of inflammatory markers. Furthermore, it elevated Bax and caspase-3 expressions, while decreasing the expressions of Bcl-2. Arsenic treatment also led to considerable histopathological impairment. However, supplementation with SCU mitigated all the arsenic-induced damage in renal tissues of the rats due to its pharmacotherapeutic properties.