Neuroprotective mechanism of Vernonia amygdalina in a rat model of neurodegenerative diseases

Abstract

The global upsurge in the prevalence of neurodegenerative diseases in recent years has been associated with increase in toxic chemical exposure and release into the biosystem, having over 46.8 million people suffer dementia worldwide. This study focused on elucidating the neuroprotective mechanism of methanol leaf extract of Vernonia amygdalina (MLVA) in nitrobenzene-induced neurodegenerative disease in rats. Thirty aged male rats were sorted into five groups of six rats each. Group A received distilled water while 100 mg/kg bw of nitrobenzene was orally administered to groups (B to E) to induce neurodegeneration. Group B (disease control) was untreated, while Group C and D were treated with oral administration of 200 and 400 mg/kg bw of MLVA respectively and group E with vitamin E for 14 days. Locomotor behaviour was analysed using video-tracking software while the midbrain, cerebrum and cerebellum of the rats were processed for biochemical analyses. Results showed that treatment of nitrobenzene-induced neurodegenerative rats with MLVA significantly (p < 0.05) increase dopamine, GSH, antioxidant enzymes levels; and decrease acetylcholinesterase activity, biomarkers of inflammatory and oxidative stress level. Also, MLVA enhanced neurobehavioural and locomotor activities in all markers assessed. Taken together, neuroprotective mechanisms of MLVA can be linked to its antioxidant, acetylcholinesterase suppression, lipid peroxidation inhibition, anti-inflammatory and neurobehavioural restoring abilities.

Keywords

• Neurodegenerative diseases
• Vernonia amygdalina
• Acetylcholinesterase
• Neurobehavioural test
• Nitrobenzene