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Comparative Study
Propofol prevents lung injury after intestinal ischemia-reperfusion by inhibiting the interaction between mast cell activation and oxidative stress.
- Weicheng Zhao, Shaoli Zhou, Weifeng Yao, Xiaoliang Gan, Guangjie Su, Dongdong Yuan, and Ziqing Hei.
- Department of Anesthesiology, The First People's Hospital of Foshan, 81 North of Rinlan Road, Foshan 528000, China; Department of Anesthesiology, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou 510630, China.
- Life Sci. 2014 Jul 17; 108 (2): 80-7.
AimsBoth mast cells and oxidative stress are involved in acute lung injury (ALI) induced by intestinal ischemia-reperfusion (IIR). The aim of this study was to investigate whether propofol could improve IIR-induced ALI through inhibiting their interaction.Main MethodsRepetitive, brief IIR or IIR+compound 48/80 was performed in adult Sprague-Dawley rats pretreated with saline, apocynin or propofol. And their lungs were excised for histology, ELISA and protein-expression measurements 2h after reperfusion.Key FindingsRats pretreated with saline developed critical ALI 2h after IIR. We found significant elevations in lung injury scores, lung wet/dry ratio and gp91phox, p47phox, intercellular cell adhesion molecule-1 protein expressions and higher level of malondialdehyde, interleukin-6 contents, and myeloperoxidase activities, as well as significant reductions in superoxide dismutase activities, accompanied with increases in mast cell degranulation evidenced by significant increases in mast cell counts, β-hexosaminidase concentrations, and tryptase expression. And the lung injury was aggravated in the presence of compound 48/80. However, pretreated with propofol and apocynin not only ameliorated the IIR-mediated pulmonary changes beyond the biochemical changes but also reversed the changes that were aggravated by compound 48/80.SignificancePropofol protects against IIR-mediated ALI, most likely by inhibiting the interaction between oxidative stress and mast cell degranulation.Copyright © 2014 Elsevier Inc. All rights reserved.
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