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Int J Clin Exp Pathol 2013;6(11):2366-2375

Original Article
Administration of dexamethasone protects mice against ischemia/reperfusion induced
renal injury by suppressing PI3K/AKT signaling

Jiong Zhang, Ying Yao, Fang Xiao, Xiaoqin Lan, Chong Yu, Ying Zhang, Cao Jiang, Juan Yang, Guangchang Pei, Yueqiang Li, Song Rong,
Shuang Hu, Junhua Li, Gang Xu

Department of Nephrology, Department of Gastroenterology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and
Technology, Wuhan, Hubei, People’s Republic of China; 3Department of Nephrology, Hannover Medical School, Hannover, Germany; The
Center for Biomedical Research, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030,
China. Equal contributors.

Received August 23, 2013; Accepted September 25, 2013; Epub October 15, 2013; Published November 1, 2013

Abstract: Dexamethasone (DEX), a ligand for glucocorticoid receptor (GR), has long been used in the clinical practice due to its anti-
inflammatory and immunosuppressive properties. Given that ischemia/reperfusion (IR)-induced renal injury is featured by the excessive
immune response; the current study is therefore designed to address the impact of dexamethasone on IR-induced renal injury, a common
disorder in the clinical settings. Precondition of mice with 4 mg/kg of dexamethasone significantly attenuated IR-induced injury as manifested
by the improved renal function along with ameliorated pathological changes and suppressed inflammatory infiltration. Mechanistic studies
revealed that dexamethasone promotes GR activation, and by which it attenuates the signals for PI3K/AKT activation. Attenuated PI3K/AKT
signaling thus suppresses inflammatory response which then protects kidneys from IR-induced injury. All together, our data support that
dexamethasone could be a good alternative therapy for prevention and treatment of IR-induced renal injury in the clinical practice.
(IJCEP1308061).

Keywords: Inflammatory response, dexamethasone, ischemia/reperfusion injury, glucocorticoid receptor, PI3K/AKT signaling

Address correspondence to: Dr. Gang Xu and Dr. Junhua Li, Department of Nephrology, Tongji Hospital, Tongji Medical College, Huazhong
University of Science and Technology, Wuhan 430030, China. Tel: 86-2783662848; Fax: 862783663187; E-mail: xugang@tjh.tjmu.edu.cn
(Gang Xu); lijunhua333@163.com (Junhua Li)