Ginkgo biloba extract mitigates behavioral deficits, oxidative stress, and hippocampal remodeling in a rat model of PTSD.

Post-traumatic stress disorder (PTSD) is associated with cognitive impairments, anxiety, fear extinction deficits, and neurobiological alterations, particularly in the hippocampus. Oxidative stress, reduced brain-derived neurotrophic factor (BDNF), and dendritic remodeling are key contributors to these dysfunctions. This study investigated whether Ginkgo biloba extract, known for its antioxidant and neuroprotective properties, could ameliorate PTSD-like symptoms and hippocampal abnormalities in male rats exposed to the single prolonged stress (SPS) model. Adult male Wistar rats were exposed to SPS and treated with Ginkgo biloba extract (20 or 200 mg/kg) for 14 days. Behavioral assessments included anxiety-like behavior, fear extinction, spatial learning and memory, and working memory. Hippocampal tissue was analyzed for oxidative stress markers (MDA, SOD, TAC), BDNF expression (Western blot), and CA3 dendritic morphology (Golgi-Cox impregnation method). SPS exposure induced marked behavioral deficits, elevated oxidative stress, reduced BDNF expression, and dendritic atrophy in CA3 pyramidal neurons. Ginkgo biloba extract, particularly at a dose of 200 mg/kg, significantly attenuated anxiety-like behaviors, facilitated fear extinction, improved memory performance, reduced oxidative damage, restored BDNF levels, and reversed dendritic retraction and branching deficits in the CA3 region of the hippocampus. These findings demonstrate that Ginkgo biloba extract exerts neuroprotective effects against trauma-induced behavioral, molecular, and structural abnormalities in a validated animal model of PTSD. While promising, these results are based on preclinical data, and further studies are necessary to determine whether similar benefits can be translated to clinical populations.