# Protective Effects of Betanin in Acute and Subacute Periods in Experimental Colitis Induced by Trinitrobenzene Sulfonic Acid

## TL;DR

This study shows that betanin reduces inflammation and oxidative stress in experimental colitis during both acute and subacute periods.

## Contribution

The novel contribution is demonstrating betanin's protective effects in both acute and subacute phases of colitis.

## Key findings

- Betanin reduced inflammatory markers like TNF-α and IL-1β in colitis.
- Betanin increased glutathione peroxidase levels, showing antioxidant effects.
- No significant change in catalase levels was observed in either period.

## Abstract

Background/Objectives: This study aims to investigate the effects of betanin, which possesses antioxidant and anti-inflammatory properties, against colitis, a disease in which inflammation and oxidative stress play a role in its pathophysiology, during the acute and subacute period. Methods: Thirty-two rats were included in the study and divided into four groups: control, colitis, 3-day betanin supplementation + colitis (bet3+colitis), and 15-day betanin supplementation + colitis (bet15+colitis). Experimental colitis was induced with trinitrobenzene sulfonic acid. Results: In the colitis group, malondialdehyde, myeloperoxidase, superoxide dismutase (SOD) inhibition rate, tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), interleukin-6, mucosal damage, and cell infiltration scores were higher than in the control group, while catalase and glutathione peroxidase (GPx) levels were lower. In the betanin supplementation groups, malondialdehyde, myeloperoxidase, TNF-α, IL-1β, mucosal damage, and cell infiltration scores were lower than in the colitis group, while GPx levels were higher. In addition, the SOD inhibition rate and interleukin-6 levels were lower in the bet15+colitis group than in the colitis group. TNF-α, IL-1β, interleukin-6, and GPx levels in the betanin groups were similar to the control group. Conclusions: Betanin supplementation demonstrated a significant anti-inflammatory effect by reducing inflammatory parameters and histopathological scores in both periods. Additionally, it exhibited a glutathione-related antioxidant effect by increasing GPx levels in both periods. However, although SOD inhibition rates decreased in the subacute period, no significant change in catalase levels was observed in either period. This indicates that it did not provide complete protection in terms of antioxidant effects in either period.