The effect of Dexpanthenol on TNBS-induced experimental colitis

Oxidative stress and inflammation are considerable risk factors in the in pathogenesis of inflammatory bowell disease (IBD). Although many studies have done on the effects of anti-inflamatory and antioxidant of dexpanthenol, it has not observed in the form of a study that conducted to investigate the effects of Trinitrobenzen Sulfonic Asid (TNBS)-induced colitis model in the rats. In accordance with this information, it is intended to invastigate the effects of dexhpanthenol through the antioxidant and anti-inflammatory mechanisms in TNBS-induced colitis. In the research, for a total of 30 rats which weights ranging from 200-250 g, divide into 4 experimental groups as DXP control (n=6), Sham control (n=8), TNBS (n=8), and TNBS+DXP (n=8). Saline was given to the Sham group and TNBS was given to the colitis group with canula as intrarectal under anesthesia. DXP was given to the DXP group without create colitis and given to the colitis group 3 days at a dose of 500 mg/kg intraperitoneally. After fasting the animals overnight and emptying the colons on the morning of experiment, inflammation was induced in the colon by the intrarectal administration of 0,8 ml of a 25 mg 2,4,6-trinitrobenzen sulfonic acid (TNBS) dissolved in 37 % ethanol using an 8 cm-long cannula under anesthesia. Animals were sacrificed on day 4. after induction of colitis and the last 10 cm of the colon was excised, opened longitudinally. Longitudinal colon segments were subjected to biochemical and histopathological examination. Statistical analyses of data were carried out using the SPSS program. Dexpanthenol caused a significant decrease in intestinal injury as determined by the histological score (p<0.05). Tissue malondialdehyde (MDA) levels were higher in the TNBS group than in the Sham and TNBS + DXP groups (p<0.05). These values were reduced in the rats treated with DXP (p <0.05). Glutathione peroxidase (GSH-Px) enzyme activity was lower in the TNBS group compared to DXP control and TNBS+DXP groups. Superoxide dismutase (SOD) enzyme activity was lower in the TNBS group compared to Shame control and TNBS groups. These antioxidant enzyme activities were increased by DXP treatment compared to TNBS group. While the increase in GSH-Px activity was significant (p<0,05), but that in the SOD was not (p>0,05). And any significant change wasnt observed between the groups in the catalase (CAT) enzyme activity. In addition, treatment with DXP also reduced elevations in myeloperoxidase (MPO) activity occuring in colonic tissue after induction of colitis. However, despite its closeness, it did not reach the significant level (p>0.05). Dexpanthenol seems to have anti-inflammatory and antioxidant properties. Therapy with DXP carries a potential to reduce the intestinal injury on TNBS-induced colitis in rats.