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Posted by star on 2022-03-30 09:17:43 Hits:69
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Xiuzhen Lei, Bihan Zhao, Jun Li, Suqin Huang, Yuhong Li, Shengmei Zhu
From: Research square

Abstract  
Dexmedetomidine (DEX), a highly selective α2 receptor agonist. DEX can inhibit the release of inflammatory factors in septic rats. It can also protect against H2O2 injury by up-regulating HIF-1α expression. The aim of this study was to explore whether DEX can up regulate HIF-1ɑ protein level and plays a role in reducing septic intestinal mucosal injury. Twenty-four Sprague Dawley (SD) rats were randomly divided into four groups of 6 rats each: the sham group, sepsis group (subjected to cecal ligation and perforation, CLP), sepsis + dexmedetomidine group (DEX group, 30 µg/kg of DEX by intraperitoneal injection 30 minutes before and 2 hours after CLP), and sepsis + DEX + HIF-1ɑ inhibitor Bay87-2243 (Bay87-2243 group, 30 µg/kg of DEX by intraperitoneal injection 30 minutes before and 2 hours after CLP and 9mg/kg of bay87-2243 by oral administration for 3 days before CLP. The HIF-1ɑ and the tight junction protein (TJs) was detected by Western blot; the plasma concentrations of diamine oxidase (DAO), intestinal fatty acid binding protein (FABP2) and D-lactic acid (D-LAC) were detected by ELISA; the morphological changes of intestinal mucosa were detected by HE staining. DEX significantly increased the expression level of HIF-1ɑ on intestinal mucosa in rats with sepsis injury, thus ameliorated intestinal mucosal pathological injury, reduced Chiu’s score, decreased intestinal mucosal permeability, and up-regulated TJs protein expression. Moreover, effect on sepsis induced intestinal mucosal injury of DEX was reversed by HIF-1ɑ inhibitor Bay87-2243. DEX could protect against sepsis-induced intestinal mucosal injury by up-regulating HIF-1ɑ expression in rats.
KEYWORDS
sepsis, dexmedetomidine, HIF-1ɑ, tight junction protein, intestinal mucosal permeability
 
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