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Journal of Toxicology
Volume 2012 (2012), Article ID 413279, 6 pages
Research Article

Protective Effect of Scutellaria litwinowii Extract on Serum/Glucose-Deprived Cultured PC12 Cells and Determining the Role of Reactive Oxygen Species

1Pharmacological Research Centre of Medicinal Plants, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
2Department of Pharmacodynamics and Toxicology, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran
3Research Center of Natural Products Safety and Medicinal Plants, North Khorasan University of Medical Sciences, Bojnurd ,01830-49504, Iran
4Medical Toxicology Research Center, School of Medicine, Mashhad University of Medical Sciences (MUMS), Mashhad, Iran

Received 1 May 2012; Accepted 24 June 2012

Academic Editor: P. J. O'Brien

Copyright © 2012 Maryam Afsharzadeh 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.


Considering the wide, positive reporting of the role of reactive oxygen species in ischemic brain injury, searching for antioxidant drugs within herbal remedies is logical. In this study, the protective effects of Scutellaria litwinowii Bornm. & Sint. on cell viability and reactive oxygen species production in cultured PC12 cells were investigated under serum/glucose-deprivation-induced cell death. After cells were seeded overnight, they were then deprived of serum/glucose for 24 h. Cells were treated with different concentrations of S. litwinowii extract (7.75–250 μg/mL). Cell viability was quantitated by MTT assay, and intracellular reactive oxygen species production was measured by flow cytometry. Serum/glucose-deprivation induced significant cell death after 24 h ( 𝑃 < 0.001). Treatment with S. litwinowii (7.75–250 μg/mL) reduced serum/glucose deprivation-induced cytotoxicity in PC12 cells after 24 h. A significant increase in intracellular reactive oxygen species production was seen following serum/glucose deprivation ( 𝑃 < 0.001). S. litwinowii (62 and 125 μg/mL, 𝑃 < 0.01) treatment reversed the increased reactive oxygen species production following ischemic insult. This demonstrates that S. litwinowii extract protects PC12 cells against serum/glucose-deprivation-induced cell death by antioxidant mechanisms, which indicates the potential therapeutic application of S. litwinowii in managing cerebral ischemic and neurodegenerative disorders.