Related Experiment Video

Updated: May 9, 2026

Ex Vivo Release of Calcitonin Gene-Related Peptide from the Trigeminovascular System in Rodents
08:39

Ex Vivo Release of Calcitonin Gene-Related Peptide from the Trigeminovascular System in Rodents

Published on: May 16, 2022

Mast Cell Stabilizer Ketotifen Inhibits Gouty Inflammation in Rats

Dur-Zong Hsu1, Pei-Yi Chu, Si-Jin Chen

  • 11Departments of Environmental and Occupational Health, National Cheng Kung University Medical College, Tainan, Taiwan; and 2Sustainable Environment Research Centre, National Cheng Kung University, Tainan, Taiwan.

American Journal of Therapeutics
|July 26, 2013
PubMed

Insights

Ketotifen, a mast cell stabilizer, reduces acute inflammation caused by monosodium urate (MSU) crystals in rats. This study suggests ketotifen may be a potential treatment for gouty inflammation by inhibiting mast cell activation and leukocyte infiltration.

Area of Science:

  • Pharmacology
  • Immunology
  • Rheumatology

Background:

  • Gout is a painful inflammatory arthritis caused by monosodium urate (MSU) crystals.
  • Mast cell activation plays a role in the inflammatory response during gout attacks.

Purpose of the Study:

  • To investigate the therapeutic effect of ketotifen, a mast cell stabilizer, on MSU crystal-induced acute inflammation.
  • To evaluate ketotifen's impact on inflammatory mediators and cellular infiltration in a rat model of gout.

Main Methods:

  • Male Wistar rats were injected with MSU crystals into an air pouch.
  • Ketotifen was administered at various doses (0, 0.1, 0.3, 1 mg/kg) one hour prior to MSU injection.
  • Histamine, leukocyte counts, mast cell activation, nitric oxide, and proinflammatory cytokines (IL-1β, IL-6) were measured 12 hours post-injection.

Main Results:

  • Ketotifen significantly inhibited MSU-induced mast cell activation and histamine release.
  • A dose-dependent reduction in leukocyte infiltration into the air pouch was observed with ketotifen treatment.
  • Ketotifen significantly decreased the production of nitric oxide, interleukin-1β, and interleukin-6 in MSU-treated rats.

Conclusions:

  • Ketotifen attenuates MSU crystal-induced acute inflammation in rats by inhibiting mast cell activation and leukocyte infiltration.
  • Ketotifen demonstrates potential as a novel therapeutic approach for managing gouty inflammation.

Related Concept Videos

Antiasthma Drugs: Mast Cell Stabilizers and Anti-IgE Drugs01:25

Antiasthma Drugs: Mast Cell Stabilizers and Anti-IgE Drugs

Asthma is a chronic respiratory condition for which new therapeutic avenues, including anti-inflammatory drugs like mast cell stabilizers and anti-IgE treatments, continue to be developed.
Mast cell stabilizers, such as cromolyn (also known as sodium cromoglycate) and nedocromil (Tilade), are effective drugs in asthma management. These stabilizers hinder histamine release by skillfully obstructing the activation of mast cells and other cellular entities. Notably, they navigate this task without...
GPCRs Regulate Adenylyl Cylase Activity01:09

GPCRs Regulate Adenylyl Cylase Activity

Some GPCRs transmit signals through adenylyl cyclase (AC), a transmembrane enzyme. AC helps synthesize second messenger cyclic adenosine monophosphate (cAMP). AC catalyzes cyclization reaction and converts ATP to cAMP by releasing a pyrophosphate. The pyrophosphate is further hydrolyzed to phosphate by the enzyme pyrophosphatase, which drives cAMP synthesis to completion. However, cAMP is rapidly degraded to 5′ AMP by the enzymes phosphodiesterase (PDE), preventing overstimulation of cells.
Two...
Open Angle Glaucoma: Treatment01:27

Open Angle Glaucoma: Treatment

In open-angle glaucoma, the iridocorneal angle remains open, but the trabecular meshwork becomes stiff, slowing down the outflow of aqueous humor. This causes a buildup of aqueous humor in the anterior chamber, leading to a sudden increase in intraocular pressure. The treatment for open-angle glaucoma focuses on reducing the elevated intraocular pressure by either decreasing the secretion of aqueous humor or increasing its outflow.
Drugs such as carbonic anhydrase inhibitors, α2- and...
Antiasthma Drugs: Leukotriene Modifiers01:19

Antiasthma Drugs: Leukotriene Modifiers

Leukotriene modifiers, or cysteinyl leukotriene receptor antagonists, are medications used to manage chronic asthma. These agents target specific inflammatory mediators produced during arachidonic acid metabolism, an essential process in generating inflammation in the body.
Leukotriene modifiers work through two distinct mechanisms:
GPCR Desensitization01:12

GPCR Desensitization

G protein-coupled receptor (GPCR) signaling plays a crucial role in cell functioning. GPCR desensitization is an equally essential process. It allows cells to respond to changing environments and regain sensitivity to new stimuli while preventing unnecessary stimulation when no longer needed. Prolonged exposure to stimuli leads to GPCR desensitization. It involves blocking the receptors from binding and activating additional G proteins. This inhibits activation of downstream effectors, thereby...