Pretreatment with dexmedetomidine ameliorates renal inflammation and oxidative stress in rats with lipopolysaccharide-induced sepsis and acute kidney injury.
- Author:
Yu-Jie CHEN
1
;
Chu-Lian GONG
;
Fang TAN
;
Shao-Li ZHOU
Author Information
- Publication Type:Journal Article
- MeSH: Acute Kidney Injury; drug therapy; Animals; Dexmedetomidine; pharmacology; Inflammation; drug therapy; Interleukin-1beta; metabolism; Kidney; drug effects; physiopathology; Lipopolysaccharides; Malondialdehyde; metabolism; Oxidative Stress; Rats; Rats, Sprague-Dawley; Sepsis; chemically induced; drug therapy; Superoxide Dismutase; metabolism
- From: Journal of Southern Medical University 2015;35(10):1472-1475
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the effects of dexmedetomidine on inflammatory reaction, oxidative stress, and renal pathologies in a rat model of lipopolysaccharide (LPS)-induced sepsis.
METHODSThirty-two SD rats were randomly divided into 4 groups, including a sham-operated group, LPS group with LPS (5 mg/kg) injection via the caudal vein 30 min before the operation, dexmedetomidine (Dex) +LPS group with additional Dex (10 µg/kg) injection via the caudal vein 10 min before LPS injection, and yohimbine+DEX+LPS group with intraperitoneal yohimbine (1 mg/kg) injection 40 min before and Dex injection 10 min before LPS injection. The levels of IL-1β, SOD and MDA in the plasma and renal tissues were determined, and the renal pathologies were examined.
RESULTSCompared with the sham-operated rats, the rats in LPS group showed significantly increased IL-1β and MDA levels and lowered SOD activity in the plasma and renal tissues (P<0.05) with obvious renal pathologies. Dex pretreatment obviously lowered IL-1β and MDA levels and enhanced SOD activity in the plasma and renal tissues in LPS-challenged rats (P<0.05), and significantly lessened LPS-induced renal pathologies.
CONCLUSIONDex can protect the rats against LPS-induced renal injury by alleviating the inflammatory reactions and cytokine oxidative stress, and this effect is mediated possibly by α2 receptors.
