Traumatic brain injury (TBI) represents a significant global public health issue, being a leading cause of morbidity, disability, and mortality across all age groups. The pathophysiology of TBI encompasses primary injury mechanisms occurring at the moment of impact and secondary injury cascades that develop over minutes to days following the initial damage. Primary injury mechanisms include contusions, lacerations, and diffuse axonal injury, while secondary injury processes involve neuroinflammation, excitotoxicity, oxidative stress, blood-brain barrier dysfunction, and mitochondrial dysfunction. Consequently, TBI patients often experience a spectrum of neurological deficits, including cognitive, motor, sensory, and emotional disturbances, significantly reducing their quality of life and independence.
Ganoderma lucidum (G. lucidum), a mushroom species belonging to the Ganodermataceae family, is renowned for its medicinal properties, particularly in Asian countries, where it is known for its vitality-enhancing and cardiotonic effects. Various bioactivities have been identified, including anti-inflammatory, antioxidant, anti-diabetic, anti-ulcer, anti-cancer, and immune-stimulatory effects.
This study aims to investigate the potential neuroprotective effects of Ganoderma lucidum on hippocampal damage resulting from traumatic brain injury. Ganoderma lucidum (Sigma Chemical Company, St. Louis, MO, USA) was used in the study. Experimental animals were anesthetized with 90 mg/kg ketamine hydrochloride and 8 mg/kg xylazine. Three groups were formed: the control group, in which a 3 cm incision was made after shaving and cleaning, the skin was sutured, and the animals were observed for 14 days; the TBI group, in which a traumatic brain injury was induced using an 18 mm diameter 50 g brass weight, and saline was administered for 14 days; and the TBI + Ganoderma lucidum group, in which Ganoderma lucidum was administered orally at a dose of 20 mg/kg for 14 days.
The results showed that in the TBI group, trauma-induced cell degeneration, vascular dilation, apoptosis, and inflammation in the pyramidal layer were observed. Degeneration was present in the synaptic nerve extensions in the plexiform layer. In the TBI + Ganoderma lucidum group, vascular dilation was reduced, axonal extensions appeared normal, and hyperplasia was observed in pyramidal neurons.
In conclusion, while the TBI group exhibited trauma-induced cell degeneration, vascular dilation, and inflammation in the pyramidal layer, the TBI + Ganoderma lucidum group showed reduced vascular dilation, normal axonal extensions, and hyperplasia in pyramidal neurons. These findings suggest that Ganoderma lucidum treatment alleviates cerebral tissue pathology following TBI.