Dexmedetomidine protects against endothelial injury in septic rats induced by cecal ligation and puncture by decreasing angiopoietin 2 and increasing vascular endothelial cadherin levels
- Peng Zhang
- Ji Peng
- Yun-Qin Ren
- Han Zheng
- Hong Yan
Affiliations: Department of Anesthesiology, Daping Hospital, Army Medical University, Chongqing 400042, P.R. China
- Published online on: December 2, 2020 https://doi.org/10.3892/etm.2020.9543
Copyright: © Zhang
et al. This is an open access article distributed under the
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The aim of the present study was to investigate the protective effect of dexmedetomidine (Dex) on endothelial injury in a cecal ligation and puncture (CLP)‑induced rat model of sepsis. A total of 36 male Sprague‑Dawley rats were divided into three groups: Sham, CLP and CLP + Dex. The wet/dry (W/D) ratio of lung weight, hematoxylin and eosin (H&E) staining of lung tissue, plasma levels of angiopoietin (Ang)1 and 2, ratio of Ang2/1 and vascular endothelial (VE)‑cadherin protein expression levels in lung tissue were determined. The W/D ratio of lung tissue in the CLP + Dex group was significantly lower than that in the CLP group (P<0.01). The H&E staining results indicated that Dex treatment reduced the levels of CLP‑induced alveolar septum widening, infiltrating white blood cells and congestion, when compared with CLP alone. In addition, the expression levels of plasma Ang2 and the Ang2/1 ratio in the CLP + Dex group were significantly lower than those of the CLP rats (P<0.01). Furthermore, the level of VE‑cadherin protein in lung tissue of the CLP + Dex group was higher than that of the CLP group (P<0.05). The results indicated that Dex had a protective effect against CLP‑induced endothelial injury, through the ability to reduce expression of the endothelial injury factor Ang2 and increase the expression of the endothelial adhesion junction factor VE‑cadherin in a septic rat model. These data suggest a potential application of Dex in the clinical treatment of sepsis.