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Lobenzarit Attenuates DSS-Induced Colitis by Reprogramming Immune Microenvironment and Mitochondrial Homeostasis
Ali Khaled1,2, Manar A Nader1,3, Marwa E Abdelmageed1,3
1Department of Pharmacology and Toxicology, Faculty of Pharmacy, Mansoura University, Mansoura 35516, Egypt.
Pharmaceuticals (Basel, Switzerland)
|June 26, 2026
Summary
Lobenzarit (Lbz) effectively treats dextran sulphate sodium (DSS)-induced colitis in mice by reducing inflammation and restoring the intestinal barrier. This compound targets the TLR4 pathway and promotes gut healing.
Area of Science:
- Gastroenterology
- Immunology
- Pharmacology
Background:
- Rising incidence of inflammatory bowel disease (IBD) globally.
- Current IBD treatments lack efficacy and have significant toxicity.
- Etiology of IBD remains incompletely understood.
Purpose of the Study:
- Investigate the therapeutic potential of Lobenzarit (Lbz) in a mouse model of colitis.
- Elucidate the underlying molecular mechanisms of Lbz's action in colitis.
Main Methods:
- Dextran sulphate sodium (DSS) model to induce colitis in mice.
- Histopathological analysis (H&E staining).
- Transmission electron microscopy (TEM).
- Biochemical assays (ELISA, PCR) to assess inflammatory markers and signaling pathways.
Main Results:
- Lobenzarit (Lbz) significantly ameliorated DSS-induced colitis symptoms.
- Lbz suppressed neutrophil infiltration and shifted macrophage polarization to an anti-inflammatory phenotype.
- Lbz inhibited TLR4 and MAPK signaling pathways, reducing key inflammatory cytokines (IL-1β, TNF-α, IFN-γ) and mediators (COX2, VEGF).
- Lbz restored intestinal barrier integrity by increasing tight junction proteins (claudin-1, occludin, ZO-1) and decreasing MALK levels.
- Lbz upregulated mitochondrial function markers (Cytochrome C oxidase II, PDH, ATP synthase) and specific macrophage markers (CD163, CD206, c-Maf, PPAR-γ).
Conclusions:
- Lobenzarit (Lbz) demonstrates significant therapeutic effects in DSS-induced colitis.
- Lbz alleviates colitis by targeting the TLR4 pathway and modulating inflammatory responses.
- Lbz may promote intestinal stem cell proliferation, contributing to tissue repair.
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