Dexmedetomidine pretreatment inhibits cerebral ischemia/reperfusion ‑induced neuroinflammation via activation of AMPK.

Dexmedetomidine pretreatment inhibits cerebral ischemia/reperfusion‑induced neuroinflammation via activation of AMPK. Mol Med Rep. 2018 Aug 03;: Authors: Wang Z, Zhou W, Dong H, Ma X, He Z Abstract Focal ischemia/reperfusion (I/R) injury induced cerebral inflammation, aggravates brain damage. The aim of the present study was to investigate the protective mechanisms of dexmedetomidine (DEX) on I/R brain injury in rats. Sprague‑Dawley rats were divided to seven experimental groups (18 rats/group): Sham surgery; middle cerebral artery occlusion (MCAO) surgery (90 min); DEX10 [10 µg/kg intraperitoneal (i.p.) injection 30 min prior to MCAO]; DEX50 (50 µg/kg i.p. 30 min prior to MCAO); DEX100 (100 µg/kg i.p. 30 min prior to MCAO); DEX50+Yohimbine [YOH; 5 mg/kg 10 min prior to DEX (50 µg/kg i.p.) administration and MCAO] and YOH (5 mg/kg 40 min prior to MCAO). At 24 h post‑MCAO surgery, neurological deficit was examined by staining damaged brain tissues with 2,3,5‑triphenyltetrazolium chloride. Neuronal apoptosis in the cerebral cortex was histologically assessed by terminal deoxynucleotidyl‑transferase‑mediated dUTP nick end labeling staining, and the expression levels of phosphorylated (p)‑AMP‑activated protein kinase (AMPK; Thr172) was detected by western blotting. In addition, the expression levels of tumor necrosis factor (TNF)‑α and interleukin (IL)‑1β were assessed by ELISA. At days 1, 2 and 5 f...
Source: Molecular Medicine Reports - Category: Molecular Biology Tags: Mol Med Rep Source Type: research