# Dose-dependent protective profile of trans-anethole in experimental traumatic brain injury in mice via modulation of apoptotic and inflammatory protein expression, and oxidative stress

## TL;DR

This study shows that trans-anethole can protect mice brains from injury by reducing harmful proteins and oxidative stress in a dose-dependent way.

## Contribution

The study demonstrates trans-anethole's dose-dependent neuroprotective effects in TBI through modulation of apoptosis, inflammation, and oxidative stress.

## Key findings

- Trans-anethole at 160 mg/kg reduced oxidative stress markers to control levels in TBI mice.
- Higher doses of trans-anethole significantly decreased pro-apoptotic and pro-inflammatory protein expression.
- The highest dose of trans-anethole fully restored immunoexpression levels to those of the control group.

## Abstract

To investigate the protective effect of trans-anethole in experimental traumatic brain injury (TBI) in mice.

Thirty-five adult mice were divided into five groups (control, TBI, TBI+A40, TBI+A80, and TBI+A160). No treatment was performed in the control group. The treated groups (TBI+A40, TBI+A80, and TBI+A160) received 40, 80 or 160 mg/kg trans-anethole treatment, respectively. At the end of the experiment, the brains of the sacrificed animals were removed, and laboratory analyses were performed.

Malondialdehyde (MDA) levels in brain tissue of TBI and TBI+A40 were significantly increased, while MDA levels of TBI+A80 and TBI were similar. TBI+A160 and control tissue MDA levels were similar (p > 0.05), significantly different from TBI (p < 0.01). Immunodensity analyses showed that there was a significant difference between the control and TBI in terms of Bax, caspase 3, tumor necrosis factor-α (TNF-α) and interleukin- (IL)-1β immunoexpression. TBI+A40 immunoexpression was similar to TBI (p > 0.05), significantly different from the control groups (p < 0.05). In TBI+A80 and TBI+A160, pro-apoptotic Bax and caspase 3, pro-inflammatory TNF-α and IL-1β levels were also significantly improved. Immunoexpression levels of TBI+A160 and control were similar (p > 0.05).

in our study, trans-anethole treatment had a dose-dependent neuroprotective potential against trauma-induced neurodegeneration.