Black pepper (Piper nigrum Linn.) has vital pharmacological properties
with profound effects on central nervous system. Neurotoxic agents like Aluminum
Chloride (AlCl3) cause the oxidative stress and result in improper processing of amyloid
proteins leading to accumulation of amyloid β plaques.
Aim: The study aimed to explore the neuroprotective potential of black pepper (BP)
extract (12.5mg/kg/day) on memory enhancement and its effect on expression of
amyloid precursor protein (APP) isoforms (APP770 and APP695) in AlCl3 induced
neurotoxicity (250mg/kg) mouse model. The study included the isolation and identification
of pure compound from BP (chavicine) which was found pharmacologically
Methods: Morris water maze test, elevated plus maze, fear conditioning, context and cue dependent test
and social preference tests were performed to investigate the learning and memory. Gene expression
(APP isoforms) and in-vitro and ex-vivo DPPH free radical scavenging activity were performed to
evaluate the role of BP.
Results: BP significantly improved memory in AlCl3 induced neurotoxicity mouse model along with effectively
decreasing the expression of APP770 (amyloidogenic) isoform and improved level of APP695
(non-amyloidogenic) in hippocampus, amygdala and cortex. Fear extinction learning was considerably
improved in BP treated group (7.83±2.03) than AlCl3 induced neurotoxicity group (39.75±4.25). In the
hippocampus, BP significantly reduced the expression of APP770 (0.37±0.05) as compared to AlCl3 induced
neurotoxicity group (0.72±0.06), and effectively increased (34.80±1.39) the percentage inhibition
of DPPH free radicals as compared to AlCl3 induced neurotoxicity group (14±2.68).
Conclusion: The study revealed that BP improves memory and chavicine is a lead compound producing
pharmacological effects of BP.