Coenzyme a-linked neuroprotection: dexpanthenol attenuates neuroinflammation, oxidative stress, and apoptosis to stabilize hippocampal function after ischemia.

Objectives

Neuroinflammation and oxidative stress following cerebral ischemia contribute to neuronal damage and cognitive dysfunction. Dexpanthenol, an antioxidant and neuroprotective derivative of pantothenic acid, may attenuate these pathological processes. This study investigated the neuroprotective effects of dexpanthenol following cerebral ischemia in rats.

Methods

Cerebral ischemia was induced using the two-vessel occlusion model, and a single intraperitoneal dose of dexpanthenol (500 mg/kg) was administered after ischemia. Behavioral assessments, including the open-field test, elevated plus maze test, forced swim test, and novel object recognition test, were performed to evaluate anxiety-like and depressive-like behaviors and cognitive performance. Enzyme-linked immunosorbent assay was used to quantify brain-derived neurotrophic factor, vascular endothelial growth factor A, hypoxia-inducible factor-1 alpha, tumor necrosis factor alpha, caspase-3, and myeloperoxidase levels. Histopathological and immunohistochemical analyses were performed to assess neuronal damage and neuroinflammatory changes.

Results

Dexpanthenol treatment increased brain-derived neurotrophic factor, vascular endothelial growth factor A, and hypoxia-inducible factor-1 alpha levels while reducing tumor necrosis factor alpha, caspase-3, and myeloperoxidase levels. Behavioral and histological findings demonstrated attenuation of neuroinflammation, neuronal loss, and cognitive deficits.

Conclusions

Dexpanthenol exerted neuroprotective effects following cerebral ischemia, accompanied by favorable changes in neurotrophic, inflammatory, apoptotic, and oxidative stress-related parameters and improvements in behavioral and histopathological outcomes. The use of a single dexpanthenol dose and an acute ischemia model represents a limitation; further dose-response and chronic studies are required to support translational relevance.