NF-kB inhibition as therapy for ulcerative colitis

NF-kB inhibition appears more effective than dexamethasone in reducing the inflammation of ulcerative colitis

Dexamethasone is a glucocorticoid – a steroidal anti-inflammatory agent commonly used in the treatment of autoimmune disease, including ulcerative colitis.

In the study below, an inhibitor of NF-kB demonstrated an anti-inflammatory effect (on a specific type of cell, outside the body) greater than that observed with dexamethasone.

The publication:

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Arch Med Res. 2008 Nov;39(8):729-34.

NF-kappaB p65 antisense oligonucleotides may serve as a novel molecular approach for the treatment of patients with ulcerative colitis.

Li Z, Zhang de K, Yi WQ, Ouyang Q, Chen YQ, Gan HT.

Summary of the abstract

BACKGROUND: Activation of NF-kB, which controls transcription of various proinflammatory cytokine genes, has been shown to play a critical role in the pathogenesis of ulcerative colitis (UC).

The aim of this study was to investigate if NF-kB p65 antisense oligonucleotides may affect the expression of NF-kappaB p65 and cytokines in patients with UC.

RESULTS: NF-kB p65 antisense oligonucleotides downregulated NF-kB, blocked the expression of IL-1beta and IL-8, and strikingly reduced the production of IL-1beta and IL-8. These effects were greater than those of dexamethasone in cultured LPMCs from patients with UC.

CONCLUSIONS: Application of NF-kB p65 antisense oligonucleotides may serve as a novel molecular approach for the treatment of patients with UC.

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