The efficiency of Cressa cretica (Linn.) extract in attenuating vancomycin-induced nephrotoxicity and oxidative stress in rabbits

The present study was aimed to assess the nephroprotective effect of Cressa cretica hydroalcoholic extract (CCE) on VAN-triggered renal toxicity in rabbits. Total phenolic and flavonoid contents found in CCE were 30.92 ± 2.93 mg GAE/g extract and 11.87 ± 1.70 mg CE/g extract, respectively. The CCE demonstrated a significant 2,2-diphenyl-1-picrylhydrazyl radical (DPPH*) scavenging ability with an IC50 value of 24.99 µg/mL. To evaluate the nephroprotective potential of CCE, thirty-six rabbits were divided into six groups (n = 6) and treated for consecutive 14 days as G-I: normal control, G-II: vehicle control (VAN 200 mg/kg, i.p.), G-III: SIL (silymarin 150 mg/kg, i.g. + VAN-treated), and G-IV to VI: CCE at 200, 400, and 600 mg/kg, i.g. + VAN-treaded groups. Blood samples were withdrawn at the 0th, 7th, and 14th days of the experiment for biochemical analysis, and renal tissues were collected at the end of experiment for antioxidant/oxidant markers and histopathological assessments. VAN significantly (P < 0.05) elevated serum levels of creatinine, blood urea nitrogen (BUN), and urea. The CCE co-administration significantly (P < 0.05) decreased the renal function markers elevated by VAN. A significantly (P < 0.05) decreased total antioxidant capacity (TAC) level, superoxide dismutase (SOD) and catalase (CAT) activities, and raised malondialdehyde (MDA) level in serum and kidney tissues were normalized in CCE-treated groups. Histopathological examination showed that CCE (600 mg/kg, i.g.) caused a mark reduction in inflammatory cell infiltration, glomerular damage, and tubular vacuolization in renal tissues of VAN-treated groups, comparable to SIL. Furthermore, CCE at 200, 400, and 600 mg/kg ameliorated VAN-induced nephrotoxicity in a dose-dependent manner. This study demonstrates the protective effect of CCE on VAN-induced nephrotoxicity by ameliorating renal function markers and suppressing oxidative stress. © 2021, The Author(s), under exclusive licence to Springer-Verlag London Ltd., part of Springer Nature.