TY - JOUR
T1 - Antioxidant effects of ginsenoside Re in cardiomyocytes
AU - Xie, Jing Tian
AU - Shao, Zuo Hui
AU - Vanden Hoek, Terry L.
AU - Chang, Wei Tien
AU - Li, Jing
AU - Mehendale, Sangeeta
AU - Wang, Chong Zhi
AU - Hsu, Chin Wang
AU - Becker, Lance B.
AU - Yin, Jun Jie
AU - Yuan, Chun Su
PY - 2006/2/27
Y1 - 2006/2/27
N2 - We have previously demonstrated that American ginseng berry extract exhibited significant protection against oxidant-mediated injury in cardiomyocytes. To extend this work, we sought to investigate the antioxidant effects of Re, a protopanaxatriols-type and single chemical integrant present in American ginseng berry extract, using the same chick cardiomyocyte model of oxidant injury as well as ESR spectroscopy in a cell-free chemical system. In cells exposed to 2 h of H2O2 (0.5 mM), pretreatment with Re (0.05, 0.1, or 0.5 mg/ml for 2 h) significantly attenuated 2′,7′-dichlorofluorescein (DCF) fluorescence by 51% (from 1345 ± 67 to 658 ± 46 a.u., P < 0.001), and remarkably reduced cell death (from 51.5 ± 3.0% to 11.8 ± 1.5%, P < 0.001, compared to the control). Similar results were also observed in cells exposed to antimycin A (100 μM), a mitochondrial electron transport chain site III inhibitor which increases endogenous oxidative stress. In the ESR study, however, Re failed to reduce the formation of the superoxide/DMPO adduct and DPPH radicals. These results suggest that ginsenoside Re functions as an antioxidant, protecting cardiomyocytes from oxidant injury induced by both exogenous and endogenous oxidants, and that its protective effects may be mostly attributed to scavenging H2O2 and hydroxyl radicals.
AB - We have previously demonstrated that American ginseng berry extract exhibited significant protection against oxidant-mediated injury in cardiomyocytes. To extend this work, we sought to investigate the antioxidant effects of Re, a protopanaxatriols-type and single chemical integrant present in American ginseng berry extract, using the same chick cardiomyocyte model of oxidant injury as well as ESR spectroscopy in a cell-free chemical system. In cells exposed to 2 h of H2O2 (0.5 mM), pretreatment with Re (0.05, 0.1, or 0.5 mg/ml for 2 h) significantly attenuated 2′,7′-dichlorofluorescein (DCF) fluorescence by 51% (from 1345 ± 67 to 658 ± 46 a.u., P < 0.001), and remarkably reduced cell death (from 51.5 ± 3.0% to 11.8 ± 1.5%, P < 0.001, compared to the control). Similar results were also observed in cells exposed to antimycin A (100 μM), a mitochondrial electron transport chain site III inhibitor which increases endogenous oxidative stress. In the ESR study, however, Re failed to reduce the formation of the superoxide/DMPO adduct and DPPH radicals. These results suggest that ginsenoside Re functions as an antioxidant, protecting cardiomyocytes from oxidant injury induced by both exogenous and endogenous oxidants, and that its protective effects may be mostly attributed to scavenging H2O2 and hydroxyl radicals.
KW - Antimycin A
KW - Antioxidant effect
KW - Cardiomyocyte
KW - ESR spectroscopy
KW - Ginsenoside Re
KW - HO
KW - Ischemia and reperfusion damage
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U2 - 10.1016/j.ejphar.2006.01.001
DO - 10.1016/j.ejphar.2006.01.001
M3 - Article
C2 - 16497296
AN - SCOPUS:33644544121
SN - 0014-2999
VL - 532
SP - 201
EP - 207
JO - European Journal of Pharmacology
JF - European Journal of Pharmacology
IS - 3
ER -