Related Experiment Video
Updated: Jan 21, 2026

Assessment of Memory Function in Pilocarpine-induced Epileptic Mice
Published on: June 4, 2020
Ondansetron enhanced diclofenac-induced nephrotoxicity in mice
Mojtaba Shakibaie1,2, Hamid Forootanfar1,2, Atoosa Ghaseminejad3
1Pharmaceutics Research Center, Institute of Neuropharmacology, Kerman University of Medical Sciences, Kerman, Iran.
Abstract:
This study was performed to investigate the effect of ondansetron, a serotonin receptor (5-HT3) antagonist, in the alleviation of diclofenac-induced kidney injuries. NMRI mice were randomly divided into six groups and treated with (A) untreated control group, (B) diclofenac (100 mg/kg), (C) ondansetron (1 mg/kg), (D to F) ondansetron (0.1, 0.5, and 1 mg/kg, respectively) and diclofenac (100 mg/kg) for last 3 days of experiment. The oxidative stress tests strongly demonstrated the negative synergistic effects of diclofenac and ondansetron, regarding the observation of dose-dependent enhancement of malondialdehyde concentration, and reduction of glutathione content, and superoxide dismutase and catalase activity. Histopathological analyses revealed dose-dependent tubular epithelial cells degeneration, outstanding mononuclear cells infiltration, clear necrosis at the papillary region of kidney, dilation, and vascular hyperemia in mice kidney tissues treated with ondansetron and diclofenac. Conclusively, these findings suggested the possible ondansetron-diclofenac interaction through the induction of oxidative stress.
Related Concept Videos
Self-Evaluation: Self-Enhancement and Self-Verification
Bioavailability Enhancement: Drug Solubility Enhancement
Bioavailability Enhancement: Drug Permeability Enhancement
Bioavailability Enhancement: Drug Stability Enhancement and GI Retention
MOSFET: Enhancement Mode
In their basic form, enhancement-mode MOSFETs are typically non-conductive when the gate-source voltage (Vgs) is zero. This default 'off' state means no...
Enhanced Elimination of Poison
Antidotes serve a crucial role in counteracting the effects of poison by inhibiting enzymes responsible for producing harmful drug metabolites. In some cases, these toxic metabolites can be neutralized by endogenous cosubstrates, which are maintained at specific concentrations to prevent interaction with cellular macromolecules and subsequent cell death.
Renal excretion is the...

