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Neuroprotective Effect of Cholecalciferol on Acute Traumatic Brain Injury

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Traumatic brain injury (TBI) results from external mechanical forces causing temporary or permanent impairments in cognitive, physical, and psychosocial functions. Cholecalciferol, a hormone with secosteroidal, neuroactive, and neurosteroidal properties, has demonstrated potential neuroprotective effects, including axon regeneration, increased axonal diameter, and improved sensory responses to metabolic stimulation. This study evaluated the histological changes in the prefrontal cortex of TBI-induced Wistar rats treated with Cholecalciferol. Forty-two Wistar rats (180–230g) were randomized into four groups, each with 12 rats, further divided into sub-groups treated or untreated with Cholecalciferol. TBI was induced using weights of 100g, 200g, and 300g. Brain tissues were harvested at 6 hours, 24 hours, and 3 days post-injury and processed using paraffin embedding and Hematoxylin-Eosin staining. Histological analyses showed normal neuronal distribution in the control group, while untreated TBI groups exhibited perinuclear halo and degenerative plaques. Cholecalciferol-treated sub-groups demonstrated varying degrees of glial cell activation, post-traumatic regeneration, and reduced tissue scarring, with significant improvements observed at higher injury severities. Findings suggest that Cholecalciferol promotes histological recovery in TBI by enhancing neuronal integrity and regeneration. Keywords: Cholecalciferol, Traumatic brain injury, Neuroprotection, Histology
Title: Neuroprotective Effect of Cholecalciferol on Acute Traumatic Brain Injury
Description:
Traumatic brain injury (TBI) results from external mechanical forces causing temporary or permanent impairments in cognitive, physical, and psychosocial functions.
Cholecalciferol, a hormone with secosteroidal, neuroactive, and neurosteroidal properties, has demonstrated potential neuroprotective effects, including axon regeneration, increased axonal diameter, and improved sensory responses to metabolic stimulation.
This study evaluated the histological changes in the prefrontal cortex of TBI-induced Wistar rats treated with Cholecalciferol.
Forty-two Wistar rats (180–230g) were randomized into four groups, each with 12 rats, further divided into sub-groups treated or untreated with Cholecalciferol.
TBI was induced using weights of 100g, 200g, and 300g.
Brain tissues were harvested at 6 hours, 24 hours, and 3 days post-injury and processed using paraffin embedding and Hematoxylin-Eosin staining.
Histological analyses showed normal neuronal distribution in the control group, while untreated TBI groups exhibited perinuclear halo and degenerative plaques.
Cholecalciferol-treated sub-groups demonstrated varying degrees of glial cell activation, post-traumatic regeneration, and reduced tissue scarring, with significant improvements observed at higher injury severities.
Findings suggest that Cholecalciferol promotes histological recovery in TBI by enhancing neuronal integrity and regeneration.
Keywords: Cholecalciferol, Traumatic brain injury, Neuroprotection, Histology.

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