Journal
LABORATORY INVESTIGATION
Volume 94, Issue 10, Pages 1147-1160Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/labinvest.2014.101
Keywords
-
Categories
Funding
- Bio & Medical Technology Development Program of the National Research Foundation (NRF) - Korean government (MEST) [2010-0019866, 2012R1A2A2A01013541]
- Korea Society of Ginseng
- Ewha Global Top5 Grant of Ewha Womans University
- Hi Seoul Science (Humanities) Fellowship - Seoul Scholarship Foundation
- National Research Foundation of Korea [2010-0019866, 2012R1A2A2A01013541] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
Ask authors/readers for more resources
Aminoglycoside-induced nephrotoxicity is one of the prevalent causes of acute kidney injury (AKI). Oxidative stress-mediated 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-2'-deoxyguanosine. Our results suggest that RGE protects the kidney from GM-induced AKI via the mechanism of modulation of oxidative stress.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available