Anil Kumar1, Archi Aggrawal2, Raghavender Pottabathini2, Arti Singh2. 1. Pharmacology Division, University Institute of Pharmaceutical Sciences, UGC Centre of Advanced Study, Panjab University, Chandigarh, India. Electronic address: kumaruips@yahoo.com. 2. Pharmacology Division, University Institute of Pharmaceutical Sciences, UGC Centre of Advanced Study, Panjab University, Chandigarh, India.
Abstract
BACKGROUND: Alzheimer's disease (AD), a common neurodegenerative disorder, recognized to be a major cause of dementia. The aim of the present study was to investigate the neuroprotective mechanisms of clove oil in intracerebroventricular (icv)-colchicine induced cognitive dysfunction in rats. METHODS: Single bilateral icv-colchicine (15μg/5μl) was administered, followed by drug treatment with clove oil (0.05ml/kg and 0.1ml/kg, ip), minocycline (25 and 50mg/kg, ip) and their combinations for a period of 21 days. Various neurobehavioral parameters followed by biochemical, acetylcholinesterase (AChE) level and mitochondrial respiratory enzyme complexes (I-IV) were assessed. RESULTS: Colchicine icv administration significantly impaired cognitive performance in Morris water maze (MWM) causes oxidative stress, raised AChE level, caused neuroinflammation and mitochondrial dysfunction as compared to sham treatment. Treatment with clove oil (0.05ml/kg and 0.1ml/kg) and minocycline (25 and 50mg/kg) alone significantly improved cognitive performance as evidenced by reduced transfer latency and increased time spent in target quadrant (TSTQ) in MWM task, reduced AChE activity, oxidative damage (reduced lipid peroxidation levels, nitrite level and restored glutathione levels) and restored mitochondrial respiratory enzyme complex (I-IV) activities as compared to icv-colchicine treatment. Further, combinations of clove oil (0.1ml/kg) with minocycline (50mg/kg) significantly modulate the neuroprotective effect of clove oil as compared to their effect alone. CONCLUSION: The present study highlights that the major neuroprotective effect of clove oil due to its mitochondrial restoring and anti-oxidant properties along with a microglial inhibitory mechanism.
BACKGROUND:Alzheimer's disease (AD), a common neurodegenerative disorder, recognized to be a major cause of dementia. The aim of the present study was to investigate the neuroprotective mechanisms of clove oil in intracerebroventricular (icv)-colchicine induced cognitive dysfunction in rats. METHODS: Single bilateral icv-colchicine (15μg/5μl) was administered, followed by drug treatment with clove oil (0.05ml/kg and 0.1ml/kg, ip), minocycline (25 and 50mg/kg, ip) and their combinations for a period of 21 days. Various neurobehavioral parameters followed by biochemical, acetylcholinesterase (AChE) level and mitochondrial respiratory enzyme complexes (I-IV) were assessed. RESULTS:Colchicine icv administration significantly impaired cognitive performance in Morris water maze (MWM) causes oxidative stress, raised AChE level, caused neuroinflammation and mitochondrial dysfunction as compared to sham treatment. Treatment with clove oil (0.05ml/kg and 0.1ml/kg) and minocycline (25 and 50mg/kg) alone significantly improved cognitive performance as evidenced by reduced transfer latency and increased time spent in target quadrant (TSTQ) in MWM task, reduced AChE activity, oxidative damage (reduced lipid peroxidation levels, nitrite level and restored glutathione levels) and restored mitochondrial respiratory enzyme complex (I-IV) activities as compared to icv-colchicine treatment. Further, combinations of clove oil (0.1ml/kg) with minocycline (50mg/kg) significantly modulate the neuroprotective effect of clove oil as compared to their effect alone. CONCLUSION: The present study highlights that the major neuroprotective effect of clove oil due to its mitochondrial restoring and anti-oxidant properties along with a microglial inhibitory mechanism.