Blocking Agent of Heme Oxygenase-1 Zinc Protoporphyria Induces Autophagy and Accelerates Oxidative Damages during Lipopolysaccharide-Induced Lung Injury in Rat
Y Gao, Y Zhang and J Zhang*
Department of Anesthesiology, Shengjing Affiliated Hospital, China Medical University, HePing District, Shenyang City, Liaoning Prov, P. R. China
- *Corresponding Author:
- J. Zhang
Department of Anesthesiology, Shengjing Affiliated Hospital
China Medical University, No. 36, SanHao Street
HePing District, Shenyang City, Liaoning Prov, P. R. China
Tel: +86-24-2389 26
E-mail: [email protected]
Received Date: April 26, 2014; Accepted Date: May 27, 2014; Published Date: June 03, 2014
Citation: Gao Y, Zhang Y, Zhang J (2014) Blocking Agent of Heme Oxygenase-1 Zinc Protoporphyria Induces Autophagy and Accelerates Oxidative Damages during Lipopolysaccharide-Induced Lung Injury in Rat. J Mol Biomark Diagn 5:183. doi:10.4172/2155-9929.1000183
Copyright: © 2014 Gao Y, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
To investigate the effect of blocking agent of heme oxygenase-1 zinc protoporphyrin (Znpp) on lipopolysaccharide (LPS)-induced autophagy in acute lung dysfunction, the rats were divided into control (C), LPS (L), LPS +Hemin (Hemin) and LPS+ZnPP (ZnPP) groups. Treatment with ZnPP induced autophagy and accelerated oxidative damages during lipopolysaccharide treatment in rat lung, LPS+ZnPP increased pathological alterations in lung tissues, the number of ballooned pulmonarycytes, serum tumor necrosis factor (TNF)-α and interleukin (IL)-6 levels, and myeloperoxidase (MPO) and malondialdehyde (MDA) levels in lung tissues (P < 0.05) but attenuated by LPS +Hemin treatment. Thus, ZnPP may aggravate LPS-induced acute lung dysfunction in rats, possibly by increasing inflammation and accelerating oxidative damages. LPS+Hemin group prolonged the median survival time and reduced lung dysfunction. Moreover, HO-1 may significantly contribute to lung protection.