eCAM Advance Access published online on January 7, 2008
eCAM, doi:10.1093/ecam/nem176
Pogostemon cablin as ROS Scavenger in Oxidant-induced Cell Death of Human Neuroglioma Cells
1Department of Herbology, College of Oriental Medicine, Dongshin University, 252 Daeho-dong, Naju, Jeonnam 520-714, 2Department of Pathology, College of Medicine, Korea University, 80 Guro-dong, Guro-gu, Seoul 152-703 and 3Department of Internal Medicine, College of Oriental Medicine, Dong-Eui University, Busan 614-714, Republic of Korea
Reactive oxygen species (ROS) have been implicated in the pathogenesis of a wide range of acute and long-term neurodegenerative diseases. This study was undertaken to examine the efficacy of Pogostemon cablin, a well-known herb in Korean traditional medicine, on ROS-induced brain cell injury. Pogostemon cablin effectively protected human neuroglioma cell line A172 against both the necrotic and apoptotic cell death induced by hydrogen peroxide (H2O2). The effect of Pogostemon cablin was dose dependent at concentrations ranging from 0.2 to 5 mg ml–1. Pogostemon cablin significantly prevented depletion of cellular ATP and activation of poly ADP-ribose polymerase induced by H2O2. The preservation of functional integrity of mitochondria upon the treatment of Pogostemon cablin was also confirmed by 3-(4,5-dimethyl-2-thiazyl)-2,5-diphenyl-2-H-tetrazolium bromide assay. Furthermore, Pogostemon cablin significantly prevented H2O2-induced release of cytochrome c into cytosol. Determination of intracellular ROS showed that Pogostemon cablin might exert its role as a powerful scavenger of intracellular ROS. The present study suggests the beneficial effect of Pogostemon cablin on ROS-induced neuroglial cell injury. The action of Pogostemon cablin as a ROS-scavenger might underlie the mechanism.
Keywords: apoptosis – H2O2 – necrosis – reactive oxygen species (ROS)
For reprints and all correspondence: Prof. Su In Cho, Department of Herbology, College of Oriental Medicine, Dongshin University, 252 Daeho-dong, Naju, Jeonnam 520-714, Republic of Korea. Tel: +82-61-330-3513; Fax: +82-61-330 3519; E-mail: sicho{at}dsu.ac.kr
*These two authors contributed equally to this work.
Received June 7, 2007; accepted November 29, 2007