지원사업
학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
커뮤니티
연구자들이 자신의 연구와 전문성을 널리 알리고, 새로운 협력의 기회를 만들 수 있는 네트워킹 공간이에요.
논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2013.10
- 수록면
- 413 - 424 (12page)
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초록· 키워드
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Korean Red Ginseng extract (KRGE) is a traditional herbal medicine utilized to prevent endothelium dysfunction in the cardiovascular system; however, its underlying mechanism has not been clearly elucidated. We here examined the pharmacological effect and molecular mechanism of KRGE on apoptosis of human umbilical vein endothelial cells (HUVECs) in a serum-deprived apoptosis model. KRGE protected HUVECs from serum-deprived apoptosis by inhibiting mitochondrial cytochrome c release and caspase-9/-3 activation. This protective effect was significantly higher than that of American ginseng extract. KRGE treatment increased antiapoptotic Bcl-2 and Bcl-XL protein expression and Akt-dependent Bad phosphorylation. Moreover, KRGE prevented serum deprivation-induced subcellular redistribution of these proteins between the mitochondrion and the cytosol, resulting in suppression of mitochondrial cytochrome c release. In addition, KRGE increased nitric oxide (NO) production via Akt-dependent activation of endothelial NO synthase (eNOS), as well as inhibited caspase-9/-3 activities. These increases were reversed by co-treatment of cells with inhibitors of eNOS and phosphoinositide 3-kinase (PI3K) and pre-incubation of cell lysates in dithiothreitol, indicating KRGE induces NO-mediated caspase modification. Indeed, KRGE inhibited caspase-3 activity via S-nitrosylation. These findings suggest that KRGE prevents serum deprivation-induced HUVEC apoptosis via increased Bcl-2 and Bcl-XL protein expression, PI3K/Akt-dependent Bad phosphorylation, and eNOS/NO-mediated S-nitrosylation of caspases. The cytoprotective property of KRGE may be valuable for developing new pharmaceutical means that limit endothelial cell death induced during the pathogenesis of vascular diseases.
목차
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
참고문헌 (35)
참고문헌 신청
1. [학술지(정기간행물)] - Cines DB / 1998 / Endothelial cells in physiology and in the pathophysiology of vascular disorders / Blood 91 : 3527 ~ 3561
2. [학술지(정기간행물)] - Stoneman VE / 2004 / Role of apoptosis in atherosclerosis and its therapeutic implications / Clin Sci (Lond) 107 : 343 ~ 354
3. [학술지(정기간행물)] - Williams TA / 2006 / Protective effect of spironolactone on endothelial cell apoptosis / Endocrinology 147 : 2496 ~ 2505
4. [학술지(정기간행물)] - Desagher S / 2000 / Mitochondria as the central control point of apoptosis / Trends Cell Biol 10 : 369 ~ 377
5. [학술지(정기간행물)] - Fujio Y / 2000 / Akt promotes survival of cardiomyocytes in vitro and protects against ischemia-reperfusion injury in mouse heart / Circulation 101 : 660 ~ 667
2. [학술지(정기간행물)] - Stoneman VE / 2004 / Role of apoptosis in atherosclerosis and its therapeutic implications / Clin Sci (Lond) 107 : 343 ~ 354
3. [학술지(정기간행물)] - Williams TA / 2006 / Protective effect of spironolactone on endothelial cell apoptosis / Endocrinology 147 : 2496 ~ 2505
4. [학술지(정기간행물)] - Desagher S / 2000 / Mitochondria as the central control point of apoptosis / Trends Cell Biol 10 : 369 ~ 377
5. [학술지(정기간행물)] - Fujio Y / 2000 / Akt promotes survival of cardiomyocytes in vitro and protects against ischemia-reperfusion injury in mouse heart / Circulation 101 : 660 ~ 667
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UCI(KEPA) : I410-ECN-0101-2014-520-002777906