Implicating the role of lycopene in restoration of mitochondrial enzymes and BDNF levels in β-amyloid induced Alzheimer׳s disease.

Lycopene has attracted significant research interest due to its beneficial therapeutic effects, which include anti-oxidant, neuro-protective and anti-cancer effects, but the mechanisms of its beneficial action are not clear so far. The present study was carried out to elucidate the neuroprotective effect of lycopene against the β-amyloid induced cognitive impairment and mitochondria oxidative damage in rats. β-amyloid (β-A1-42) was administered through intracerebroventricular (ICV) by using stereotaxic instrument in male Wistar rats. Lycopene (2.5 and 5mg/kg) was administrated for three weeks. Behavioral performances were conducted during the study. The rats were sacrificed on the 21st day following the last behavioral test and cytoplasmic fractions of hippocampus were prepared for the quantification of acetylcholinesterase, oxidative stress parameter, mitochondrial enzymes, and inflammatory mediator like TNF-α, Il-6 activities, caspase-3 and BDNF. ICV β-A1-42 resulted in poor memory retention in Morris water maze and caused marked oxidative stress as indicated by significant increase in oxidative, mitochondria damage, TNF-α, IL-6 and Caspase-3 activity. We also found that β-A1-42 induced animal altered BDNF level than control animals. Chronic administration of lycopene resulted in an improvement in memory retention, attenuation of mitochondrial-oxidative damage, reduced neuro-inflammation and restoration of BDNF level in β-A1-42 treated rats. These studies indicated that lycopene helps to protect β-A1-42 induced cognitive dysfunction and modulates amyloidogenesis.