Maesa ramentacea Leaf Extract Protects Against Gentamicin‐Induced Nephrotoxicity in Wistar Rats by Modulating Renal Oxidative Stress, Inflammation and Apoptosis

Background Gentamicin‐induced nephrotoxicity continues to be a significant clinical concern, while effective and safe protective options remain limited. The nephroprotective potential of Maesa ramentacea has not yet been explored. To address this gap, the present study investigated the ethanolic leaf extract of M. ramentacea (MR‐LEE) for its effects on gentamicin‐induced kidney injury in Wistar rats. Methods GC‐MS profiling was employed to identify bioactive metabolites. Rats were categorised into five groups: control, gentamicin (100 mg/kg), gentamicin combined with silymarin (100 mg/kg), gentamicin combined with MR‐LEE (200 mg/kg) and gentamicin combined with MR‐LEE (400 mg/kg). Renal biomarkers, oxidative stress indicators, inflammatory and apoptotic markers and histopathological evaluations were conducted. Results Nine bioactive metabolites have been identified using GC‐MS. Gentamicin significantly elevated serum creatinine (1.17 ± 0.13 mg/dL), urea (69.9 ± 3.44 mg/dL), uric acid (5.52 ± 1.15 mg/dL) and LDH (4770 ± 480 U/L) compared to the control group ( p = 0.0001). MR‐LEE at 400 mg/kg significantly decreased creatinine (0.65 ± 0.05 mg/dL), urea (45.3 ± 2.66 mg/dL) and LDH (4250 ± 380 U/L) ( p = 0.0001), approaching the levels observed with silymarin. Gentamicin increased TNF‐α (58.8 ± 4.6 pg/mg), IL‐6 (53.1 ± 2.23 pg/mg) and caspase‐3 (37.6 ± 2.44 ng/mg) ( p = 0.0001), but MR‐LEE 400 mg/kg significantly decreased these levels to 33.1 ± 2.3, 29.5 ± 2.33 and 21.5 ± 1.66, respectively ( p = 0.005). MR‐LEE restored antioxidant enzyme levels (GSH, SOD and CAT) and reduced lipid peroxidation, as evidenced by histological analyses showing decreased tubular necrosis and nearly normal renal architecture. Conclusion MR‐LEE appeared to exert a notable, dose‐dependent nephroprotective effect. Future research should focus on isolating active components and elucidating molecular mechanisms to facilitate translational use.