Galangin significantly mitigated doxorubicin-induced liver and kidney damage by reducing IL-6 and 8-OHdG levels while restoring AQP-1 expression in rats.
Does galangin mitigate doxorubicin-induced hepatorenal toxicity in a rat model?
Galangin shows potential as a therapeutic agent to mitigate doxorubicin-induced hepatorenal toxicity through antioxidant and anti-inflammatory mechanisms.
Absolute Event Rate: 0% vs 0%
ABSTRACT This study investigates the protective effects of galangin (GAL) against doxorubicin (Dox)‐induced hepatorenal toxicity in a rat model, focusing on oxidative stress, inflammation, and key markers, including interleukin‐6 (IL‐6), 8‐hydroxydeoxyguanosine (8‐OHdG), and aquaporin‐1 (AQP‐1). Male Sprague‐Dawley rats were divided into four groups: Control, Dox, Dox+GAL 50 mg/kg, and Dox+GAL 100 mg/kg. GAL significantly attenuated Dox‐induced damage by reducing IL‐6 and 8‐OHdG levels, restoring AQP‐1 expression, and improving histopathological profiles. Biochemical analysis demonstrated GAL's antioxidant activity, evidenced by elevated levels of glutathione (GSH), superoxide dismutase (SOD), and catalase (CAT), alongside decreased levels of malondialdehyde (MDA). These findings suggest GAL as a potential therapeutic agent for mitigating Dox‐induced organ toxicity, with broader implications for conditions involving oxidative stress and inflammation.
Akdemi̇r et al. (Mon,) reported a other. Galangin significantly mitigated doxorubicin-induced liver and kidney damage by reducing IL-6 and 8-OHdG levels while restoring AQP-1 expression in rats.