Related Experiment Video

Updated: Jan 21, 2026

Assessment of Memory Function in Pilocarpine-induced Epileptic Mice
13:34

Assessment of Memory Function in Pilocarpine-induced Epileptic Mice

Published on: June 4, 2020

8.8K

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.

Journal of Biochemical and Molecular Toxicology
|July 24, 2019
PubMed

Insights

Ondansetron worsens diclofenac-induced kidney injury by increasing oxidative stress. This drug combination led to significant kidney damage in mice, highlighting a negative interaction.

Area of Science:

  • Pharmacology
  • Toxicology
  • Nephrology

Background:

  • Diclofenac is a common nonsteroidal anti-inflammatory drug (NSAID) known to cause kidney injury.
  • Ondansetron is a serotonin 5-HT3 receptor antagonist used to prevent nausea and vomiting.

Purpose of the Study:

  • To investigate the potential protective or detrimental effects of ondansetron on diclofenac-induced kidney injury.
  • To explore the underlying mechanisms, particularly oxidative stress, involved in this interaction.

Main Methods:

  • NMRI mice were administered diclofenac and varying doses of ondansetron.
  • Oxidative stress markers including malondialdehyde, glutathione, superoxide dismutase, and catalase were assessed.
  • Kidney tissues were analyzed histopathologically for signs of damage.

Main Results:

  • A synergistic negative effect was observed between diclofenac and ondansetron.
  • Increased malondialdehyde and decreased glutathione, superoxide dismutase, and catalase levels indicated heightened oxidative stress.
  • Histopathology revealed dose-dependent tubular degeneration, inflammation, necrosis, and vascular hyperemia in the kidneys.

Conclusions:

  • Ondansetron exacerbates diclofenac-induced kidney injury.
  • The interaction appears to be mediated through the induction of oxidative stress.
  • Caution is advised when co-administering ondansetron and diclofenac due to potential nephrotoxicity.
Keywords:
interactionkidneyoxidative stressserotonin receptor

More Related Videos

Restraint to Induce Stress in Mice and Rats03:48

Restraint to Induce Stress in Mice and Rats

Published on: December 6, 2024

3.2K
In vivo Imaging of Optic Nerve Fiber Integrity by Contrast-Enhanced MRI in Mice11:38

In vivo Imaging of Optic Nerve Fiber Integrity by Contrast-Enhanced MRI in Mice

Published on: July 22, 2014

13.9K

Related Concept Videos

Self-Evaluation: Self-Enhancement and Self-Verification03:00

Self-Evaluation: Self-Enhancement and Self-Verification

Social psychologists have documented that feeling good about ourselves and maintaining positive self-esteem is a powerful motivator of human behavior (Tavris & Aronson, 2008). In the United States, members of the predominant culture typically think very highly of themselves and view themselves as good people who are above average on many desirable traits (Ehrlinger, Gilovich, & Ross, 2005). Often, our behavior, attitudes, and beliefs are affected when we experience a threat to our...
5.7K
Bioavailability Enhancement: Drug Solubility Enhancement01:16

Bioavailability Enhancement: Drug Solubility Enhancement

Body:Bioavailability is a critical factor in determining a drug's effectiveness. It refers to the proportion of a drug that enters the circulation when introduced into the body and is, as a result, able to have an active effect. Enhancing bioavailability is essential for drugs with poor solubility, as it can significantly impact their therapeutic efficacy. Various methods are employed to increase the solubility of drugs, thereby enhancing their bioavailability.Micronization and nanonization are...
226
Bioavailability Enhancement: Drug Permeability Enhancement01:27

Bioavailability Enhancement: Drug Permeability Enhancement

Body:After oral administration, poor permeability often limits the rate at which drugs are absorbed through the intestinal epithelium. Enhancing drug permeability is crucial for effective therapy, and several strategies have been developed to overcome this challenge.One effective strategy involves the use of lipid-based formulations. These formulations enhance dissolution and solubility, targeting physiological mechanisms to increase drug absorption. This includes stimulating bile salt...
193
Bioavailability Enhancement: Drug Stability Enhancement and GI Retention01:05

Bioavailability Enhancement: Drug Stability Enhancement and GI Retention

Body:Improving a drug's stability in the gastrointestinal (GI) tract is paramount for enhancing its bioavailability and therapeutic effectiveness. Various strategies are employed to protect the drug from the harsh gastric milieu and to ensure its release and absorption at the desired site within the GI tract.Polymer coatings are one such method used to shield drugs from the stomach's acidic environment. By preventing premature drug release, these coatings improve the bioavailability of unstable...
202
MOSFET: Enhancement Mode01:22

MOSFET: Enhancement Mode

Enhancement-mode MOSFETs are pivotal components in electronics, distinguished by their capacity to act as highly efficient switches. They are part of the larger family of metal-oxide Semiconductor Field-Effect Transistors (MOSFETs). They are available in two types: p-channel and n-channel, each tailored to specific polarity operations.
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...
801
Enhanced Elimination of Poison01:26

Enhanced Elimination of Poison

Poison can be effectively removed from the gastrointestinal (GI) tract through various decontamination procedures.
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...
876