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An efficient protocol that could enhance the generation of quality non-brain-sourced neural stem cells (NSCs) for the treatment of neurodegenerative diseases (ND) is essential. This study aims to evaluate the effect of Centella asiatica (CA), which has been consumed traditionally as memory tonic, in enhancing the transdifferentiation potential of full-term amniotic fluid stem cells (AFSCs), a highly neurogenic stem cell, into NSCs. Treatment with CA extract was found to increase the expression of NSC protein markers, generate more good quality neurospheres and enhance the expression of selected neuronal markers. These findings strongly suggest that CA has the potential to enhance NSCs transdifferentiated from AFSCs, demonstrating the remarkable ability of non-brain-sourced stem cells derived from merely discarded fluid to transform into brain cells. [ABSTRACT FROM AUTHOR]

Autophagy plays a protective role in the retinal pigment epithelium (RPE) by eliminating damaged organelles in response to reactive oxygen species (ROS). Dual-specificity protein phosphatase 6 (DUSP6), which belongs to the DUSP subfamily, works as a negative-feedback regulator of the extracellular signal-regulated kinase (ERK) pathway. However, the complex interplay between DUSP6 and autophagy induced by ROS in RPE is yet to be investigated. To investigate the relationship between DUSP6 and autophagy, we exposed the ARPE-19 cell line and C57BL/6N mice to sodium iodate (NaIO3) as an oxidative stress inducer. Our data showed that the inhibition of DUSP6 activity promotes autophagy flux through the ERK pathway via the upregulation of immunoblotting expression in ARPE-19 cells. Live imaging showed a significant increase in autophagic flux activities, which suggested the restoration autophagy after treatment with the DUSP6 inhibitor. Furthermore, the mouse RPE layer exhibited an irregular structure and abnormal deposits following NaIO3 injection. The retina layer was recovered after being treated with DUSP6 inhibitor; this suggests that DUSP6 inhibitor can rescue retinal damage by restoring the mouse retina's autophagy flux. This study suggests that the upregulation of DUSP6 can cause autophagy flux malfunctions in the RPE. The DUSP6 inhibitor can restore autophagy induction, which may serve as a potential therapeutic approach for retinal degeneration disease. [ABSTRACT FROM AUTHOR]