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논문 기본 정보

자료유형
학술저널
저자정보
Eun-Hye Kim (Sungkyunkwan University) In-Hye Kim (Sungkyunkwan University) Jung-Ah Ha (Sungkyunkwan University) Kwang-Tae Choi (Kyung Hee University) Suhkneung Pyo (Sungkyunkwan University) Dong-Kwon Rhee (Sungkyunkwan University)
저널정보
고려인삼학회 Journal of Ginseng Research Journal of Ginseng Research Vol.37 No.3
발행연도
2013.7
수록면
315 - 323 (9page)

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초록· 키워드

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Ginseng is known to have antistress effects. Previously, red ginseng (RG) was shown to repress stress-induced peptidyl arginine deiminase type IV (PADI4) via estrogen receptor β (ERβ) in the brain, thus inhibiting brain cell apoptosis. Moreover, tumor necrosis factor (TNF)-α plays a critical role in immobilization (IMO) stress. However, the signaling pathway of RG-mediated repressesion of inflammation is not completely understood. In this study, we determined how RG modulated gene expression in stressed brain cells. Since secretion of TNF-α is modulated via TNF-α converting enzyme (TACE) and nuclear factor (NF)-κB, we examined the inflammatory pathway in stressed brain cells. Immunohistochemistry revealed that TACE was induced by IMO stress, but RG repressed TACE induction. Moreover, PADI4 siRNA repressed TACE expression compared to the mock transfected control suggesting that PADI4 was required for TACE expression. A reporter assay also revealed that H₂O₂ oxidative stress induced NF-κB in neuroblastoma SK-N-SH cells, however, RG pretreatment repressed NF-κB induction. These findings were supported by significant induction of nitric oxide and reactive oxygen species (ROS) by oxidative stress, which could be repressed by RG administration. Taken together, RG appeared to repress stress-induced PADI4 via TACE and NF-κB in brain cells thus preventing production of ROS and subsequently protecting brain cells from apoptosis.

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INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES

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