Abstract
Bacopa monnieri L. Wettst. (BM) is a botanical component of Ayurvedic medicines and of dietary supplements used worldwide for cognitive health and function. We previously reported that administration of BM alcoholic extract (BME) prevents trimethyltin (TMT)-induced cognitive deficits and hippocampal cell damage and promotes TMT-induced hippocampal neurogenesis. In this study, we demonstrate that administration of BME improves spatial working memory in adolescent (5-week- old) healthy mice but not adult (8-week-old) mice. Moreover, improved spatial working memory was retained even at 4 weeks after terminating 1-week treatment of adolescent mice. One-week BME treatment of adolescent mice significantly enhanced hippocampal BrdU incorporation and expression of genes involved in neurogenesis determined by RNAseq analysis. Cell death, as detected by histochemistry, appeared not to be significant. A significant increase in neurogenesis was observed in the dentate gyrus region 4 weeks after terminating 1-week treatment of adolescent mice with BME. Bacopaside I, an active component of BME, promoted the proliferation of neural progenitor cells in vitro in a concentration-dependent manner via the facilitation of the Akt and ERK1/2 signaling. These results suggest that BME enhances spatial working memory in healthy adolescent mice by promoting hippocampal neurogenesis and that the effects of BME are due, in significant amounts, to bacopaside I.
Highlights
The capacity of neural stem cells to proliferate and differentiate into neuronal cells in the brain contributes to prevention and recovery from memory loss and other neurodegenerative diseases [1,2]
Our studies suggested that bacopaside I, a major triterpenoid component of BM extracts (BME), has a significant role in the effect of BME, since it protected neuronal cells from oxygen- and glucose-deprivation-induced damage via protein kinase C (PKC) and phosphatidylinositol-3 kinase (PI3K)/Akt mechanisms in organotypic hippocampal slice cultures [8]
When spatial working memory of the same animal groups was determined on day 28 after consecutive daily administration of BME, no significant difference was observed between the BME-treated group and vehicle-treated group (t(19) = 0.443, p = 0.663, water-treated group vs. BME-treated group)
Summary
The capacity of neural stem cells to proliferate and differentiate into neuronal cells in the brain contributes to prevention and recovery from memory loss and other neurodegenerative diseases [1,2]. Promotion of neurogenesis in the hippocampal dentate gyrus region by enhancing the self-regenerative ability of neuronal stem cells offers potential for maintaining and improving cognitive function [7]. We recently reported that BME ameliorates trimethyltin (TMT)-induced cognition dysfunction by protecting hippocampal neurons from TMT-induced lesions and partly by promoting neurogeneration in the hippocampal dentate gyrus region [15]. These results prompted us to hypothesize that BME may have the potential to improve cognitive function in healthy animals by promoting neurogenesis in the hippocampus. The results demonstrate that BME enhancement of cognitive performance is accompanied by promotion of neurogenesis in the hippocampal dentate gyrus of adolescent mice, but not adult mice
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