TY - JOUR
T1 - Renoprotective effect of red ginseng in gentamicin-induced acute kidney injury
AU - Shin, Hyun Soo
AU - Yu, Mina
AU - Kim, Mijin
AU - Choi, Hack Sun
AU - Kang, Duk Hee
N1 - Funding Information:
This research was supported by the Bio & Medical Technology Development Program of the National Research Foundation (NRF) funded by the Korean government (MEST) (2010-0019866, 2012R1A2A2A01013541), the Korea Society of Ginseng (2008), the Ewha Global Top5 Grant 2013 of Ewha Womans University and Hi Seoul Science (Humanities) Fellowship funded by Seoul Scholarship Foundation.
Publisher Copyright:
© 2014 USCAP, Inc All rights reserved.
PY - 2014/1/1
Y1 - 2014/1/1
N2 - Aminoglycoside-induced nephrotoxicity is one of the prevalent causes of acute kidney injury (AKI). Oxidative stressmediated apoptosis of renal tubular cells is known to be a major mechanism of renal injury. Red ginseng extract (RGE) has been reported to possess antioxidant and immune-modulatory activities. We investigated the effect of RGE on gentamicin (GM)-induced apoptosis and oxidative stress in cultured renal tubular cells and animal model of GM-induced AKI. GM induced the generation of reactive oxygen species (ROS) with an increase in NADPH oxidase (NOX) activity and mitochondrial oxidation in NRK-52E cells that were ameliorated with RGE. GM-induced apoptosis of NRK-52E cells, which was associated with an increased expression of mitochondrial Bax, cytosolic cytochrome c, and cleaved caspase-9 and-3, along with a decrease in bcl-2 expression, was also blocked by RGE. In an animal model of GM-induced AKI, RGE treatment significantly attenuated renal dysfunction, cell apoptosis, and tubular damage. RGE ameliorated ROS production in rats with GM-induced AKI, as demonstrated by an increase in the reduced form of glutathione in renal cortex and a decrease in urinary excretion of 8-hydroxy-20-deoxyguanosine. Our results suggest that RGE protects the kidney from GM-induced AKI via the mechanism of modulation of oxidative stress.
AB - Aminoglycoside-induced nephrotoxicity is one of the prevalent causes of acute kidney injury (AKI). Oxidative stressmediated apoptosis of renal tubular cells is known to be a major mechanism of renal injury. Red ginseng extract (RGE) has been reported to possess antioxidant and immune-modulatory activities. We investigated the effect of RGE on gentamicin (GM)-induced apoptosis and oxidative stress in cultured renal tubular cells and animal model of GM-induced AKI. GM induced the generation of reactive oxygen species (ROS) with an increase in NADPH oxidase (NOX) activity and mitochondrial oxidation in NRK-52E cells that were ameliorated with RGE. GM-induced apoptosis of NRK-52E cells, which was associated with an increased expression of mitochondrial Bax, cytosolic cytochrome c, and cleaved caspase-9 and-3, along with a decrease in bcl-2 expression, was also blocked by RGE. In an animal model of GM-induced AKI, RGE treatment significantly attenuated renal dysfunction, cell apoptosis, and tubular damage. RGE ameliorated ROS production in rats with GM-induced AKI, as demonstrated by an increase in the reduced form of glutathione in renal cortex and a decrease in urinary excretion of 8-hydroxy-20-deoxyguanosine. Our results suggest that RGE protects the kidney from GM-induced AKI via the mechanism of modulation of oxidative stress.
UR - http://www.scopus.com/inward/record.url?scp=84920987297&partnerID=8YFLogxK
U2 - 10.1038/labinvest.2014.101
DO - 10.1038/labinvest.2014.101
M3 - Article
C2 - 25111692
AN - SCOPUS:84920987297
VL - 94
SP - 1147
EP - 1160
JO - Laboratory Investigation
JF - Laboratory Investigation
SN - 0023-6837
IS - 10
ER -