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Standardized extract of Bacopa monniera (BESEB CDRI‐08) attenuates contextual associative learning deficits in the aging rat's brain induced by D‐galactose
Author(s) -
Prisila Dulcy Charles,
Singh Hemant K.,
Preethi Jayakumar,
Emmanuvel Rajan Koilmani
Publication year - 2012
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.23080
Subject(s) - synaptic plasticity , synaptophysin , associative learning , glutathione peroxidase , endocrinology , postsynaptic density , medicine , pharmacology , antioxidant , neuroprotection , chemistry , neuroscience , biology , superoxide dismutase , biochemistry , receptor , immunohistochemistry
In this study, we examined the neuroprotective effect of standardized Bacopa monniera extract (BME: BESEB CDRI‐08) against the D‐galactose (D‐gal)‐induced brain aging in rats. Experimental groups were subjected to contextual‐associative learning task. We found that the administration of BME in the D‐gal‐treated group attenuated contextual‐associative learning deficits; the individuals showed more correct responses and retrieved the reward with less latency. Subsequent analysis showed that the BME administration significantly decreased advance glycation end product (AGE) in serum and increased the activity of antioxidant response element (ARE) and the antioxidant enzymes superoxide dismutase (SOD), glutathione peroxidase (GSH‐Px), and nuclear transcription factor NF‐E2‐related factor 2 ( Nrf2 ), accompanied by a reduction in the level of serotonin (5‐HT) in the hippocampus. The BME treatment also reversed D‐gal‐induced brain aging by upregulating the levels of the presynaptic proteins synaptotagmin I (SYT1) and synaptophysin (SYP) and the postsynaptic proteins Ca 2+ /calmodulin dependent protein kinase II (αCaMKII) and postsynaptic density protein‐95 (PSD‐95) in the hippocampus during synaptic plasticity. A significant finding is that the D‐gal‐ + BME‐treated rats exhibited more correct responses in contextual‐associative learning than D‐gal alone‐treated rats. Our findings suggest that BME treatment attenuates D‐gal‐induced brain aging and regulates the level of antioxidant enzymes, Nrf2 expression, and the level of 5‐HT, which was accompanied by concomitantly increased levels of synaptic proteins SYT1, SYP, αCaMKII, p‐αCaMKII, and PSD‐95. © 2012 Wiley Periodicals, Inc.