Raffia hookeri Ethanolic Pulp Extract Ameliorated Neuronal Damage and Brain Oxidative Stress Following...

Area of Science:

• Neuroscience
• Pharmacology
• Toxicology

Background:

• Traumatic brain injury (TBI) is a significant cause of mortality and morbidity.
• Current treatments for TBI are limited, highlighting the need for novel therapeutic strategies.
• Raphia hookeri possesses known antioxidant properties, suggesting potential neuroprotective benefits.

Purpose of the Study:

• To investigate the ameliorative effects of Raphia hookeri ethanol extract (RHEE) on experimentally induced acute traumatic brain injury (TBI) in a rat model.
• To assess the impact of RHEE on oxidative stress markers and histological damage following TBI.
• To evaluate RHEE's efficacy in both sharp trauma brain injury (STBI) and blunt trauma brain injury (BTBI) models.

Main Methods:

• Thirty-six female Wistar rats were subjected to either STBI or BTBI using a modified weight drop technique.
• RHEE was administered orally for seven days post-injury at a dose of 100 mg/kg.
• Blood, brain tissue, and biochemical markers (MDA, GSH, SOD, CAT) were analyzed at various time points post-trauma.

Main Results:

• Trauma significantly reduced relative brain weight and altered white blood cell differentials (increased lymphocytes, decreased neutrophils).
• Both STBI and BTBI elevated malondialdehyde (MDA) levels and decreased glutathione (GSH) levels, superoxide dismutase (SOD), and catalase (CAT) activities.
• RHEE administration significantly reduced oxidative damage and histological evidence of neuronal damage, including hemorrhage, in both STBI and BTBI groups.

Conclusions:

• Raphia hookeri ethanol extract demonstrates significant neuroprotective effects against acute traumatic brain injury in rats.
• RHEE effectively mitigates oxidative stress and reduces neuronal damage associated with both sharp and blunt force brain trauma.
• These findings suggest RHEE as a potential therapeutic agent for managing TBI.