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Effects of Sunghyangchungisan(SHCS) on oxidant-induced cell death in human neuroglioma cells
김나리,권정남,김영귄 대한한의학회 2005 대한한의학회지 Vol.26 No.2
Objective: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 whether Sunghyangchungisan (SHCS), a well-known prescription in Korean traditional medicine, might have beneficial effects on ROS-induced brain cell injury. Methods:Human neuroglioma cell line A172 and H2O2 were employed as an experimental model cell and oxidant. Results;SHCS effectively protected the cells against both the necrotic and apoptotic cell death induced by H2O2. The effect of SHCS was dose-dependent at concentrations ranging from 0.2 to 5 mg/㎖. SHCS significantly prevented depletion of cellular ATP and activation of poly (ADP-ribose) polymerase induced by H2O2. It also helped mitochondria to preserve its functional integrity estimated by MTT reduction ability. Furthermore, SHCS significantly prevented H2O2-induced release of cytochrome c into cytosol. Determination of intracellular ROS showed that SHCS might exert its role as a powerful scavenger of intracellular ROS. Conclusion:The present study provides clear evidence for the beneficial effect of SHCS on ROS-induced neuoglial cell injury. The action of SHCS as an ROS-scavenger might underlie the mechanism. Objective: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 whether Sunghyangchungisan (SHCS), a well-known prescription in Korean traditional medicine, might have beneficial effects on ROS-induced brain cell injury. Methods:Human neuroglioma cell line A172 and H2O2 were employed as an experimental model cell and oxidant. Results;SHCS effectively protected the cells against both the necrotic and apoptotic cell death induced by H2O2. The effect of SHCS was dose-dependent at concentrations ranging from 0.2 to 5 mg/㎖. SHCS significantly prevented depletion of cellular ATP and activation of poly (ADP-ribose) polymerase induced by H2O2. It also helped mitochondria to preserve its functional integrity estimated by MTT reduction ability. Furthermore, SHCS significantly prevented H2O2-induced release of cytochrome c into cytosol. Determination of intracellular ROS showed that SHCS might exert its role as a powerful scavenger of intracellular ROS. Conclusion:The present study provides clear evidence for the beneficial effect of SHCS on ROS-induced neuoglial cell injury. The action of SHCS as an ROS-scavenger might underlie the mechanism.
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