Abstract
Chinese herbal medicines (CHMs) have been used to treat human diseases for thousands of years. Among them, Ginkgo biloba is reported to be beneficial to the nervous system and a potential treatment of neurological disorders. Since the presence of adult neural stem cells (NSCs) brings hope that the brain may heal itself, whether the effect of Ginkgo biloba is on NSCs remains elusive. In this study, we found that Ginkgo biloba extract (GBE) and one of its main ingredients, ginkgolide B (GB) promoted cell cycle exit and neuronal differentiation in NSCs derived from the postnatal subventricular zone (SVZ) of the mouse lateral ventricle. Furthermore, the administration of GB increased the nuclear level of β-catenin and activated the canonical Wnt pathway. Knockdown of β-catenin blocked the neurogenic effect of GB, suggesting that GB promotes neuronal differentiation through the Wnt/β-catenin pathway. Thus, our data provide a potential mechanism underlying the therapeutic effect of GBE or GB on brain injuries and neurodegenerative disorders.
Highlights
In mammals, neural stem cells (NSCs) in the subventricular zone (SVZ) of the lateral ventricle and the subgranule zone (SGZ) of the hippocampal dentate gyrus (DG) give rise to new neurons in the olfactory bulb (OB) and DG throughout adulthood, respectively[1]
We reveal that Ginkgo biloba extract (GBE) and ginkgolide B (GB), a component of GBE, promote neuronal differentiation through the Wnt pathway in postnatal NSCs
We showed that GB promoted cell cycle withdrawal and induced neuronal differentiation (Figs 2 and 3)
Summary
Neural stem cells (NSCs) in the subventricular zone (SVZ) of the lateral ventricle and the subgranule zone (SGZ) of the hippocampal dentate gyrus (DG) give rise to new neurons in the olfactory bulb (OB) and DG throughout adulthood, respectively[1]. Strategies to enhance neurogenesis of endogenous NSCs could be a promising therapeutic treatment for relieving brain injuries or neurodegenerative disorders. Neuroblasts migrate along the rostral migratory stream (RMS) to the OB and differentiate into mature neurons[1]. Many signaling pathways, such as Notch, Sonic Hedgehog (Shh), Wnt/β-catenin and extracellular signal-regulated kinase (ERK) pathways activated by neurotrophic factors have been demonstrated to regulate self-renewal and neurogenesis of NSCs8–12. Since CHMs have been shown to be beneficial to various neurological diseases, such as AD and HD, it prompts us to screen CHMs and components of CHMs for promoting neurogenesis. It has been suggested that GBE prevents cell death and promotes hippocampal neurogenesis www.nature.com/scientificreports/. GBE treatment significantly increased the number of Tuj1positive cells. It is important to identify the effective components in GBE for treating neurological disorders
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
