Format

Send to

Choose Destination
See comment in PubMed Commons below
Int J Clin Exp Pathol. 2013 Oct 15;6(11):2366-75. eCollection 2013.

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

Author information

  • 1Department of Nephrology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology Wuhan, Hubei, People's Republic of China.

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.

KEYWORDS:

Inflammatory response; PI3K/AKT signaling; dexamethasone; glucocorticoid receptor; ischemia/reperfusion injury

PMID:
24228098
PMCID:
PMC3816805
[PubMed - indexed for MEDLINE]
Free PMC Article
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for PubMed Central
    Loading ...
    Write to the Help Desk