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Updated: Jun 10, 2026
Murine Colitis Modeling using Dextran Sulfate Sodium (DSS)
Published on: January 20, 2010
Impaired nitrergic innervation in rat colitis induced by dextran sulfate sodium
Y Mizuta1, H Isomoto, T Takahashi
1Second Department of Internal Medicine, Nagasaki University School of Medicine, Nagasaki, Japan.
Background & Aims:
The pathophysiological role of neuronal nitric oxide synthase (nNOS) in colitis remains unknown.
Methods:
We investigated colonic transit, nonadrenergic, noncholinergic (NANC) relaxation, nNOS activity, and nNOS synthesis in the myenteric plexus in dextran sulfate sodium (DSS)-induced colitis in rats.
Results:
Oral administration of 5% DSS for 7 days induced predominant distal colitis and delayed colonic transit. In the proximal colon, carbachol-, sodium nitroprusside-, and electrical field stimulation (EFS)-induced responses were not different between control and DSS-treated rats. In the distal colon, EFS-evoked cholinergic contraction, NANC relaxation, and orphanin FQ-induced contraction were significantly impaired in DSS-treated rats compared with those in control rats, but carbachol- and sodium nitroprusside-induced responses remained intact in DSS-treated rats. The number of nNOS-immunopositive cells, catalytic activity of NOS, and nNOS synthesis in the colonic wall were significantly reduced in the distal colon of DSS-treated rats. In contrast, the number of PGP 9.5-immunopositive cells and PGP 9.5 synthesis in the colonic wall remained intact in the distal colon of DSS-treated rats.
Conclusions:
These results suggest that impaired NANC relaxation in the distal colon is associated with reduced activity and synthesis of nNOS in the myenteric plexus in DSS-induced colitis.
