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Ceramide has been involved in cell death and acted as a lipid mediator of stress responses. Elevation of ceramide level was reported to occur in oxidative stress and lead to cell death in many cell types. This study was undertaken to elucidate a protective role of ginsenoside Rg1 in cell death induced by oxidative stress. When LLC-PK1 cells were treated with H₂O₂ at a concentration of 400 μM for 5 hr, cell death was observed and a released LDH activity indicative of cytotoxicity was increased. H₂O₂ exposure to LLC-PK1 cells was shown to elevate the content of total ceramide by approximately 200% compared to control cells. Ceramide level was hypothesized to be a key to a reversal of cell death to survival. Ginsenoside Rg1 at the concentrations ranging from 12.5 to 250 μM protected LLC-PK1 cells from cell death induced by H₂O₂ at 400 μM for 5 hr, and decreased the ceramide level relative to H₂O₂. Ginsenoside Rg1 inhibited neutral human ceramidase by 71% of controls, while sphingomyelinase was not inhibited. These results suggest that ginsenoside Rg1 show the protection against cell death via the modulation of ceramide metabolism, and ceramide may be a promising therapeutic target for human diseases related to cell death.

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Abstract
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
ACKNOWLEDGEMENT
REFERENCES

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UCI(KEPA) : I410-ECN-0101-2009-524-015598914