Abstract
BackgroundThis study investigates the protective effects of turmeric (Curcuma longa, CL) on acetic acid-induced colitis in rats.MethodInflammatory bowel disease (IBD) was induced in male Wistar rats by intra-rectal administration of 1 ml of 4 % acetic acid at 8 cm proximal to the anus for 30 s. Curcuma longa (CL) powder, (1, 10, or 100 mg/kg/day) was administered for either 3 days before or after IBD for 7 days. The body weight, macroscopic and microscopic analysis of the colon of CL-treated IBD rats and that of control rats (no IBD, no CL) were performed on 0 day, 2, 4 and 7th day. Myeloperoxidase (MPO), IL-23 and glutathione levels in control, untreated and treated rats were measured by ELISA.ResultsCL significantly (P < 0.05) improved IBD-induced reduction in mean body weight and mean macroscopic ulcer score. Administration of CL also significantly (P < 0.01) reduced the mean microscopic ulcer score when compared to untreated IBD control. Intake of CL by rats resulted in a significant (P < 0.05) increase in the mean serum glutathione level compared to untreated control. CL reduced both MPO and IL-23 levels in the colonic mucosa of the rat.ConclusionCL improved body weight gain, mean macroscopic and microscopic ulcer scores in the colon of rats suffering from acetic acid-induced IBD. CL reduced both MPO and IL-23 in the mucosa of the colon. The increase in the mean serum glutathione level may help in the reduction of oxidative stress associated with IBD.
Highlights
This study investigates the protective effects of turmeric (Curcuma longa, curcuma longa (CL)) on acetic acid-induced colitis in rats
Administration of CL significantly (P < 0.01) reduced the mean microscopic ulcer score when compared to untreated inflammatory bowel disease (IBD) control
Intake of CL by rats resulted in a significant (P < 0.05) increase in the mean serum glutathione level compared to untreated control
Summary
This study investigates the protective effects of turmeric (Curcuma longa, CL) on acetic acid-induced colitis in rats. Genetic deletion or antibody-mediated neutralization of interleukin 12 (IL-12) led to amelioration of intestinal inflammation in a number of different models [4, 5]. It was shown that IL-23 and not IL-12 is the key molecule in the development of a variety of inflammatory conditions including intestinal inflammation [6]. The demonstration of the association of genetics in the IL-23 pathway in multiple chronic inflammatory disorders, including inflammatory bowel disease (IBD), has coincided with significant advances in the understanding of its key role in host defense and organ-specific autoimmunity. Evidence for the importance of IL-23 pathway in IBD has come from mouse models of IBD, in which IL-23 deficiency or blockade protects the mice from the disease [7, 8], but human IBD as well [9,10,11]
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