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Int. J. Mol. Sci. 2014, 15(9), 15426-15442; doi:10.3390/ijms150915426

Inhibition of Autophagy via Activation of PI3K/Akt Pathway Contributes to the Protection of Ginsenoside Rb1 against Neuronal Death Caused by Ischemic Insults

1
Department of Neurology, First Hospital of Jilin University, Changchun 130021, China
2
Department of Pediatrics, Anzhen Hospital of Capital University of Medical Sciences, Beijing 10029, China
3
Department of Pathology, First Hospital of Jilin University, Changchun 130021, China
4
Department of Neurosurgery, First Hospital of Jilin University, Changchun 130021, China
5
Department of Pediatrics, First Hospital of Jilin University, Changchun 130021, China
These authors contributed equally to this work.
*
Authors to whom correspondence should be addressed.
Received: 9 July 2014 / Revised: 20 August 2014 / Accepted: 25 August 2014 / Published: 1 September 2014
(This article belongs to the Section Biochemistry, Molecular and Cellular Biology)
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Abstract

Lethal autophagy is a pathway leading to neuronal death caused by transient global ischemia. In this study, we examined the effect of Ginsenoside Rb1 (GRb1) on ischemia/reperfusion-induced autophagic neuronal death and investigated the role of PI3K/Akt. Ischemic neuronal death in vitro was induced by using oxygen glucose deprivation (OGD) in SH-SY5Y cells, and transient global ischemia was produced by using two vessels occlusion in rats. Cellular viability of SH-SY5Y cells was assessed by MTT assay, and CA1 neuronal death was evaluated by Hematoxylin-eosin staining. Autophagic vacuoles were detected by using both fluorescent microscopy in combination with acridine orange (AO) and Monodansylcadaverine (MDC) staining and transmission electronic microscopy. Protein levels of LC3II, Beclin1, total Akt and phosphor-Akt at Ser473 were examined by western blotting analysis. GRb1 inhibited both OGD and transient ischemia-induced neuronal death and mitigated OGD-induced autophagic vacuoles in SH-SY5Y cells. By contrast, PI3K inhibitor LY294002 counteracted the protection of GRb1 against neuronal death caused by either OGD or transient ischemia. LY294002 not only mitigated the up-regulated protein level of phosphor Akt at Ser473 caused by GRb1, but also reversed the inhibitory effect of GRb1 on OGD and transient ischemia-induced elevation in protein levels of LC3II and Beclin1. View Full-Text
Keywords: autophagy; OGD; transient global ischemia; Ginsenoside Rb1; PI3K/Akt autophagy; OGD; transient global ischemia; Ginsenoside Rb1; PI3K/Akt
This is an open access article distributed under the Creative Commons Attribution License (CC BY 3.0).

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Luo, T.; Liu, G.; Ma, H.; Lu, B.; Xu, H.; Wang, Y.; Wu, J.; Ge, P.; Liang, J. Inhibition of Autophagy via Activation of PI3K/Akt Pathway Contributes to the Protection of Ginsenoside Rb1 against Neuronal Death Caused by Ischemic Insults. Int. J. Mol. Sci. 2014, 15, 15426-15442.

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