Research Papers:

Peroxiredoxin 6 overexpression attenuates lipopolysaccharide-induced acute kidney injury

Dong Hun Lee, Ju Ho Park, Sang Bae Han, Do Young Yoon, Yu Yeon Jung and Jin Tae Hong _

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Oncotarget. 2017; 8:51096-51107. https://doi.org/10.18632/oncotarget.17002

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Dong Hun Lee1,3, Ju Ho Park1, Sang Bae Han1, Do Young Yoon2, Yu Yeon Jung4 and Jin Tae Hong1

1College of Pharmacy and Medical Research Center, Chungbuk National University, Osong-eup, Heungduk-gu, Cheongju, Chungbuk, 361-951, Republic of Korea

2Department of Bioscience and Biotechnology, Bio/Molecular Informatics Center, Konkuk University, Hwayang-dong, Gwangjin-gu, Seoul 143-701, Republic of Korea

3Department of Pediatrics, School of Medicine, Emory University, Atlanta, GA 30329, USA

4Department of Dental Hygiene, Gwangyang Health Sciences University, Gwnagyang, Jeonnam 57764, Republic of Korea

Correspondence to:

Jin-Tae Hong, email: [email protected]

Yu Yeon Jung, email: [email protected]

Keywords: peroxiredoxin 6, acute kidney injury, reactive oxygen species, MAP kinase

Received: February 10, 2016     Accepted: February 20, 2017     Published: April 10, 2017


Peroxiredoxin 6 (PRDX6) is a member of the PRDX family of antioxidant enzymes and correlated with inflammatory response. Therefore, we investigated the role of PRDX6 during lipopolysaccharide (LPS)-induced acute kidney injury. Both 3 months aged PRDX6-overexpressing transgenic mice (PRDX6 mice) and wild type (WT) mice had acute renal injury induced by intraperitoneal injection of LPS (10 mg/kg)., PRDX6 mice showed decreased mortality and renal injury following LPS challenge compared to WT mice. Furthermore, infiltration of macrophages, T-cells and neutrophils, and the number of apoptotic cells were more decreased by LPS treatment in PRDX6 mice than in WT mice. Because LPS induces reactive oxygen species (ROS) production which induces inflammation through c-Jun N-terminal Kinase (JNK) and p38 MAPK activation, we investigated ROS concentration and MAPK signaling pathway in the kidney of PRDX6 mice. As expected, LPS-induced oxidative stress was attenuated, and p38 MAPK and JNK activation was decreased in the kidney of PRDX6 mice. Inhibitory effect of PRDX6 on LPS-induced apoptosis and MAPK activation in the primary renal proximal tubular cells were overcome by treatment with PRDX6 inhibitor or hydrogen peroxide. These results suggest that PRDX6 overexpression inactivates p38 MAPK and JNK pathway through decrease LPS-induced ROS concentration in the kidney, resulting in inhibition of renal apoptosis and leukocyte infiltration and led to attenuation of LPS-induced acute kidney injury.

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