Effect of mesenchymal stem cells on expression of cyclophilin A in lipopolysaccharide-induced acute lung injury rat
- Author:
Hai-qing WU
1
Author Information
1. Department of Intensive Care Unit, Longhua Hospital
- Publication Type:Journal Article
- Keywords:
Acute lung injury;
Cyclophilin A;
Lipopolysaccharide;
Mesenchymal stem cell
- From:
Journal of International Pharmaceutical Research
2012;39(5):425-429
- CountryChina
- Language:Chinese
-
Abstract:
Objective To observe the expression of cyclophilin A(CyPA) in lung tissues of lipopolysaccharide (LPS) induced acute lung injury rat and the influence of mesenchymal stem cells (MSC) on the activity of CyPA. Methods Ninety SD rats were randomly divided into 5 groups (18 in each group); model group: 5mg/kg LPS were given through tail vein injection; stem cells control group; bone mairow MSC(BMSC)2 × 106/ml 0.5 ml were given through tail vein injection; nomial control group; equivalent normal saline were given through tail vein injection; stem cells treatment groups; 5 mg/kg LPS + BMSC 2 × 106/ml, 1 × 106/ml 0.5 ml were given through tail vein injection. The lung tissues of rats which is put to death were collected at 6, 24 and 72 hours after molding. Determine the content of tumor necrosis factor (TNT)-α interleukin (IL)-1β and myeloperoxidase (MPO) inferior part of right lung tissues and expression of CyPA were determined by Western blot and RT-PCR. Results Compared with normal control group, the level of MPO, TNF-α, IL-1β and CyPA were increased signiticantly in model group and stem cells treatment group. The expression of CyPA mRNA of lung tissnes in 1 × 106 stem cells treatment group were decreased significantly than those in model group (P < 0. 05). Conclusion The CyPA may participate in the morbility of lipopolysaccharide-induction acute lung injury rat. Bone marrow MSC of mice have protective effect on endotoxin induced acute lung injury, and the mechanism may be related with the reducing of the expression of CyPA. © 2006 Editorial office of Foreign Medical Sciences.