Abstract
The herb Centella asiatica has long been considered a memory tonic. A recent review found no strong evidence for improvement of cognitive function, suggesting negative results were due to limitations in dose, standardization and product variation. We used a standardized extract of C. asiatica (ECa 233) to study behavioral, cellular and molecular effects on learning and memory enhancement. ECa 233 (10, 30, and 100 mg/kg) was given orally to normal rats twice a day for 30 days. We used the Morris water maze to test spatial learning and performed acute brain slice recording to measure changes of synaptic plasticity in the hippocampus, a core brain region for memory formation. Plasticity-related protein expressions (NR2A, NR2B, PSD-95, BDNF and TrkB) in hippocampus was also measured. Rats receiving 10 and 30 mg/kg doses showed significantly enhanced memory retention, and hippocampal long-term potentiation; however, only the 30 mg/kg dose showed increased plasticity-related proteins. There was an inverted U-shaped response of ECa 233 on memory enhancement; 30 mg/kg maximally enhanced memory retention with an increase of synaptic plasticity and plasticity-related proteins in hippocampus. Our data clearly support the beneficial effect on memory retention of a standardized extract of Centella asiatica within a specific therapeutic range.
Highlights
Aging population is a global problem, affecting both patient’s and caregiver’s health, while patient mental decline is a major burden in caregiving
Enhanced memory performance was measured by results of the Morris water maze task, and synaptic enhancement in the hippocampus was assessed by measuring long-term potentiation magnitude, while expression of plasticity-related proteins following N-methyl-D-aspartate receptor (NMDAR)-signaling activation was examined by western blot analysis
We investigated the memory enhancing effect of a standardized extract of Centella asiatica (ECa 233) on learning and memory in normal rats
Summary
Aging population is a global problem, affecting both patient’s and caregiver’s health, while patient mental decline is a major burden in caregiving. ECa 233 demonstrated neuroprotective effects by attenuating the learning and memory deficit induced by transient bilateral occlusion of common carotid arteries (T2VO)[9] or cerebral infusion of amyloid beta peptide 25–35 fragments (Aβ25–35)[10]. These neuroprotective effects were proposed to act through anti-oxidant and anti-inflammatory mechanisms of ECa 233. BDNF promotes the growth of original synapses and formation of new synapses through binding with its receptor, tyrosine kinase B (TrkB) This is the basis of synaptic plasticity in learning and memory formation[12]. We confirmed distribution of major bioactive constituents in the hippocampus and plasma using the liquid chromatography tandem-mass spectrometry (LC-MS/MS) technique
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