The antioxidant EPC-K1 attenuates renal ischemia-reperfusion injury in a rat model.

Abstract:

BACKGROUND:Acute kidney injury (AKI) occurs frequently in the intensive care unit. A primary cause is renal ischemia/reperfusion (I/R) injury, during which excess reactive oxygen species (ROS) are produced. ROS subsequently damage renal cells, leading to the development of AKI. Here, we investigated whether renal I/R injury could be attenuated by the antioxidant EPC-K1. METHODS:We divided male Wistar rats into the following three groups: (1) a renal I/R group, (2) an EPC-K1 + renal I/R group and (3) a control group. Rats were sacrificed 24 h after treatment (I/R or sham). To measure oxidative stress in renal tissue, histological examinations were performed and serum levels of blood urea nitrogen (BUN) and creatinine were measured. The antioxidant action of EPC-K1 was also evaluated in RAW264.7 cells stimulated with antimycin A. RESULTS:Serum BUN and creatinine levels were elevated in the I/R group; however, this increase was significantly attenuated by EPC-K1 in the EPC-K1 + I/R group. Renal tissue injury was also significantly lower in the EPC-K1 + I/R group compared with the I/R group. In vitro experiments showed that EPC-K1 significantly attenuated the generation of ROS induced by antimycin A. CONCLUSION:In our study, EPC-K1 was able to attenuate AKI due to renal I/R by reducing oxidative stress. These results suggest that EPC-K1 may be effective against various types of I/R injury.

journal_name

Am J Nephrol

authors

Yamamoto S,Hagiwara S,Hidaka S,Shingu C,Goto K,Kashima K,Noguchi T

doi

10.1159/000327820

subject

Has Abstract

pub_date

2011-01-01 00:00:00

pages

485-90

issue

6

eissn

0250-8095

issn

1421-9670

pii

000327820

journal_volume

33

pub_type

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