Hao Ling, Junbing Mao, Bing Xu, Yaning Shi, Jicang Wang
Cadmium (Cd) exposure in occupational settings poses significant nephrotoxic risks, yet effective preventive strategies remain limited. This study investigated the protective effects of Naringenin (Nar) against Cd-induced nephrotoxicity. Twenty-four male SD rats (4 weeks old) were randomly assigned to control group, Cd group, Nar group, and Cd+ group for 14 days. Histopathological damage characterized by tubular necrosis and inflammatory infiltration. Cd exposure significantly impaired renal function, as evidenced by elevated serum uric acid and creatinine levels, increased oxidative stress markers (renal glutathione and malondialdehyde accumulation). Molecular analysis confirmed Cd-induced apoptosis through dysregulation of key apoptotic markers: downregulation of anti-apoptotic Bcl-2 and upregulation of pro-apoptotic Bax at both mRNA and protein levels, accompanied by increased cytochrome c release and activation of Caspase-9 and Caspase-3. These findings were further supported by TUNEL staining, which showed increased apoptosis in renal tubular cells. This study supports the potential application of naringin in alleviating cadmium-induced nephrotoxicity.