L-Arginine reduces acetic acid-induced colitis

What is it about?

The transcription factor, nuclear factor-κB (NF-κB) is a key inducer of inducible nitric oxide synthase (iNOS) gene expression. The aim of the present study is to investigate the potential protective effect of L-arginine (NO precursor) and aminoguanidine (iNOS inhibitor) against acetic acid (AA) -induced colitis in rats and the potential role of NF-κB . Colitis was induced by intra-rectal inoculation of rats with 4% acetic acid for 3 consecutive days. The effect of L-Arginine (Arg) and aminoguanidine (AG) on nitric oxide (NO) levels was assessed by Greiss assay and protein expression of NF-κB / p65 and iNOS was also investigated by immunohistochemistry (IHC). Slides were examined using ImageJ and results reported as the percent area positive for each marker. Intra-rectal acetic acid caused a significant increase in body weight loss and colon weights. L-arginine at 100 mg/day for 7 days prior to induction of colitis diminished the changes in both body weight loss and colon weights. Moreover, Arg attenuated the colonic tissues macroscopic and microscopic damage induced by acetic acid. In addition, i.p. AG 100 mg/ Kg administered during and after induction of colitis recovered the colonic ulcerative lesion induced by AA. L-arginine can protect against colonic inflammation; an effect that probably attributed to its NO donating property resulting in modulatory effects on the expression of NF-κB / p65 in the colon tissues. Our results suggested that Arg may reduce the inflammation associated with colitis as confirmed by histopathological investigations. L-arginine may inhibit AA-induced colitis via NF-κB/NO pathway.

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