Abstract：
: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.
journal_name
Eur J Pharmacoljournal_title
European journal of pharmacologyauthors
Prakash A,Kumar Adoi
10.1016/j.ejphar.2014.07.036subject
Has Abstractpub_date
2014-10-15 00:00:00pages
104-11eissn
0014-2999issn
1879-0712pii
S0014-2999(14)00573-1journal_volume
741pub_type
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