JoVE - Journal of Visualized Experiments
JoVE Visualize
Contact Us

The protective role of nicardipine in dextran sulfate sodium-induced colitis in mice: Modulating inflammation and apoptosis

  • 0Department of Pharmacology and Toxicology, College of Pharmacy, University of Baghdad, Baghdad 10047, Iraq.
Toxicology Reports +

|

September 25, 2025

|

September 25, 2025

View abstract on PubMed

Summary

This summary is machine-generated.

Nicardipine, a calcium channel blocker, effectively reduced inflammation, oxidative stress, and apoptosis in a mouse model of ulcerative colitis (UC). These findings suggest nicardipine

Area Of Science

  • Gastroenterology and Immunology
  • Pharmacology and Therapeutics

Background

  • Ulcerative colitis (UC) is a chronic inflammatory bowel disease characterized by inflammation, oxidative stress, and epithelial cell apoptosis.
  • Nicardipine, a dihydropyridine calcium channel blocker, possesses anti-inflammatory and anti-apoptotic properties, but its efficacy in UC is not well-established.

Purpose Of The Study

  • To evaluate the therapeutic effects of nicardipine on dextran sulfate sodium (DSS)-induced colitis in a mouse model.
  • To investigate the impact of nicardipine on inflammatory, oxidative, and apoptotic pathways in colitis.

Main Methods

  • BALB/c mice were induced with colitis using DSS and treated with varying doses of nicardipine or 5-aminosalicylate (ASA).
  • Disease severity was assessed via body weight, disease activity index (DAI), and colon length.
  • Colonic gene expression (Nlrp3, TNF-α, IL-17, TNFSF10), protein levels (caspase-3, caspase-8, BAX, BCL-2), serum markers (MDA, MPO, GPX-1, occludin, PGE-2), and histology were analyzed.

Main Results

  • Nicardipine demonstrated dose-dependent improvements in body weight, DAI, and colon length, and significantly downregulated pro-inflammatory markers.
  • Nicardipine treatment reduced apoptosis markers (caspase-3, BAX), increased anti-apoptotic BCL-2, restored antioxidant GPX-1, and decreased oxidative stress markers (MDA, MPO).
  • Nicardipine preserved epithelial integrity, maintained occludin levels, and reduced prostaglandin E2 (PGE-2), with histological evidence of reduced mucosal injury.

Conclusions

  • Nicardipine effectively attenuates DSS-induced colitis by suppressing inflammation, oxidative stress, and apoptosis.
  • These findings support nicardipine's potential as a therapeutic agent for ulcerative colitis.
  • Further research is needed to elucidate its precise molecular mechanisms and clinical applicability.

Keywords: