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.

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

METHODS

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.

RESULTS

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).

CONCLUSION

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