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Advances in Pharmacological Sciences
Volume 2016 (2016), Article ID 3073078, 5 pages
http://dx.doi.org/10.1155/2016/3073078
Research Article

Protective Effect of Diospyros kaki against Glucose-Oxygen-Serum Deprivation-Induced PC12 Cells Injury

1Neurocognitive Research Center, School of Medicine, Mashhad University of Medical Sciences, Mashhad 917794-8564, Iran
2Pharmacological Research Center of Medicinal Plants, School of Medicine, Mashhad University of Medical Sciences, Mashhad 917794-8564, Iran
3Department of Pharmacology, School of Medicine, Mashhad University of Medical Sciences, Mashhad 917794-8564, Iran
4Anesthesiology and Critical Care Research Center, Shiraz University of Medical Sciences, Shiraz, Iran

Received 21 November 2015; Accepted 10 January 2016

Academic Editor: Masahiro Oike

Copyright © 2016 Fatemeh Forouzanfar et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Ischemic cerebrovascular disease is one of the most common causes of death in the world. Recent interests have been focused on natural antioxidants and anti-inflammatory agents as potentially useful neuroprotective agents. Diospyros kaki (persimmon) has been shown to exert anti-inflammatory, antioxidant, and antineoplastic effects. However, its effects on ischemic damage have not been evaluated. Here, we used an in vitro model of cerebral ischemia and studied the effects of hydroalcoholic extract of peel (PeHE) and fruit pulp (PuHE) of persimmon on cell viability and markers of oxidative damage mainly intracellular reactive oxygen species (ROS) induced by glucose-oxygen-serum deprivation (GOSD) in PC12 cells. GOSD for 6 h produced significant cell death which was accompanied by increased levels of ROS. Pretreatment with different concentrations of PeHE and PuHE (0–500 μg/mL) for 2 and 24 h markedly restored these changes only at high concentrations. However, no significant differences were seen in the protection against ischemic insult between different extracts and the time of exposure. The experimental results suggest that persimmon protects the PC12 cells from GOSD-induced injury via antioxidant mechanisms. Our findings might raise the possibility of potential therapeutic application of persimmon for managing cerebral ischemic and other neurodegenerative disorders.