Abstract
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.