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Cited 9 time in webofscience Cited 11 time in scopus
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Renoprotective Effects of a Highly Selective A3 Adenosine Receptor Antagonist in a Mouse Model of Adriamycin-induced Nephropathyopen access

Authors
Min, Hye SookCha, Jin JooKim, KitaeKim, Jung EunGhee, Jung YeonKim, HyunwookLee, Ji EunHan, Jee-YoungJeong, Lak ShinCha, Dae RyongKang, Young Sun
Issue Date
Sep-2016
Publisher
KOREAN ACAD MEDICAL SCIENCES
Keywords
Adriamycin; Nephropathy; Adenosine Receptor Antagonist; Mouse Model
Citation
JOURNAL OF KOREAN MEDICAL SCIENCE, v.31, no.9, pp.1403 - +
Indexed
SCIE
SCOPUS
KCI
Journal Title
JOURNAL OF KOREAN MEDICAL SCIENCE
Volume
31
Number
9
Start Page
1403
End Page
+
URI
https://scholarworks.korea.ac.kr/kumedicine/handle/2020.sw.kumedicine/6121
DOI
10.3346/jkms.2016.31.9.1403
ISSN
1011-8934
Abstract
The concentration of adenosine in the normal kidney increases markedly during renal hypoxia, ischemia, and inflammation. A recent study reported that an A3 adenosine receptor (A3AR) antagonist attenuated the progression of renal fibrosis. The adriamycin (ADX)-induced nephropathy model induces podocyte injury, which results in severe proteinuria and progressive glomerulosclerosis. In this study, we investigated the preventive effect of a highly selective A3AR antagonist (LJ1888) in ADX-induced nephropathy. Three groups of six-week-old Balb/c mice were treated with ADX (11 mg/kg) for four weeks and LJ1888 (10 mg/kg) for two weeks as following: 1) control; 2) ADX; and 3) ADX + LJ1888. ADX treatment decreased body weight without a change in water and food intake, but this was ameliorated by LJ1888 treatment. Interestingly, LJ1888 lowered plasma creatinine level, proteinuria, and albuminuria, which had increased during ADX treatment. Furthermore, LJ1888 inhibited urinary nephrin excretion as a podocyte injury marker, and urine 8-isoprostane and kidney lipid peroxide concentration, which are markers of oxidative stress, increased after injection of ADX. ADX also induced the activation of proinflammatory and profibrotic molecules such as TGF-beta 1, MCP-1, PAI-1, type IV collagen, NF-kappa B, NOX4, TLR4, TNF alpha, IL-1 beta, and IFN-gamma, but they were remarkably suppressed after LJ1888 treatment. In conclusion, our results suggest that LJ1888 has a renoprotective effect in ADX-induced nephropathy, which might be associated with podocyte injury through oxidative stress. Therefore, LJ1888, a selective A3AR antagonist, could be considered as a potential therapeutic agent in renal glomerular diseases which include podocyte injury and proteinuria.
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Cha, Dae Ryong
Ansan Hospital (Department of Nephrology and Hypertension, Ansan Hospital)
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