Assessment of Ameliorative Potential of Co-enzyme Q10 (Co_Q10) Supplementation in Brain Derived Neurotrophic Factor (BDNF) and Serum Acetylcholinesterase (AChE) Altered Rat Models

Abstract

Neurodegenerative diseases affect millions of people worldwide. And the levels of some biomolecules like brain-derived neurotrophic factor (BDNF) and acetylcholinesterase (AChE) are known to play significant roles in different neurodegenerative diseases. The present study therefore assessed the ameliorative potential of Co-enzyme Q10 (CoQ10 or Co_Q10) supplementation in altered levels of BDNF and AChE in thioacetamide (TAA) induced hepatic encephalopathy (HE) in male Wistar rat models. Male Wistar rats weighing 250±30 g were used for the study and were randomly separated into six different groups of twenty rats each. The groups included Group 1-control and received 1ml of normal saline (intraperitoneally―ip), Group 2 received only 200 mg/kg TAA (ip) twice weekly, Group 3 received 5mg/kg Co_Q10, daily per oral (po), Group 4 received 10mg/kg Co_Q10 daily (po), Group 5 received 200 mg/kg TAA (ip) twice weekly and 5mg/kg Co_Q10 (po) daily and Group 6 received 200 mg/kg TAA (ip) twice weekly and 10mg/kg Co_Q10 (po) daily. At the end of weeks 3, 6, 9 and 12 of treatment, blood samples were immediately transferred into appropriately labeled blood sample bottles containing anticoagulant. Numerical data obtained from the study were subjected to statistical analyses using analyses of variance and Post Hoc tools of the statistical package for social sciences 21.0V software. The result indicated significantly (P<0.05) depressed level of BDNF and significantly (P<0.05) raised level of AChE in the TAA only treated Group 2 when compared to Group 1 and the rest groups. It was observed that, both of Co_Q10 only treated and Co_Q10 + TAA treated groups had marked (P<0.05) elevated and depressed levels of BDNF and AChE respectively in the study models. Supplementations with different doses of Co_Q10 (5 and 10mg/kg) indicated significant improvement in TAA altered levels of BDNF and AChE in a mammalian model.