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Secondary injury is a potentially modifiable factor of outcome in traumatic brain injury. This study aimed to investigate thymoquinone's effects on trauma-induced neuronal damage. Eighteen adult female Sprague–Dawley rats were assigned into three groups following ketamine and xylazine anaesthesia ( n  = 6): Control, Trauma, Trauma + Thymoquinone. First dose of thymoquinone was administered three hours after the trauma. The trauma group showed significant oedema, vascular congestion, and ischaemia. Also, caspase-3 activity and malondialdehyde content of brain tissue was significantly increased, and Na,K-ATPase activity and glutathione levels were significantly reduced. Thymoquinone significantly reduced oedema, vascular congestion, ischaemia, and caspase-3 activity compared with the trauma group. While Na,K-ATPase activity and glutathione levels was similar to the Control group, malondialdehyde content was similar to the trauma group. This study showed that low dose thymoquinone exhibited a neuroprotective effect following severe traumatic brain injury, if administered within three hours of injury. Similar levels of glutathione and malondialdehyde suggest no antioxidant effect. Significant reduction in oedema and ischaemia in the neuron cells and partially preserved activity of Na,K-ATPase suggest that thymoquinone protects mitochondrial functions and energy levels of the neuronal cells following severe traumatic brain injury.

Protective effect of thymoquinone in preventing trauma-related damage: an experimental study