Involvement of metallothionein in the protection of lung ischemic preconditioning.
- Author:
Dong-Wu XU
1
;
Lu SHI
;
Xu-Guang JIA
;
Xiao-Ying QIAN
;
Lan-Lan TANG
;
Yan-Hua ZHANG
;
Yang WANG
;
Wan-Tie WANG
Author Information
1. Department of Pathophysiology of Wenzhou Medical College, Wenzhou 325035, China.
- Publication Type:Journal Article
- MeSH:
Animals;
Ischemic Preconditioning;
methods;
Lung;
blood supply;
metabolism;
Male;
Metallothionein;
physiology;
Random Allocation;
Rats;
Rats, Sprague-Dawley;
Reperfusion Injury;
metabolism;
prevention & control
- From:
Acta Physiologica Sinica
2010;62(5):465-468
- CountryChina
- Language:Chinese
-
Abstract:
The aim of the present study was to investigate whether metallothionein was involved in the protection of lung ischemic preconditioning (IP) against lung ischemia-reperfusion (I/R) injury. Adult male Sprague-Dawley rats were randomly divided into 3 groups based upon the intervention (n=8): control group (C), lung I/R group (I/R), lung I/R+IP group (IP). At the end of the experiment, the content of metallothionein was tested in lung tissue. Blood specimens collected from the arteria carotis were tested for the contents of malondialdehyde (MDA), the activities of superoxide dismutase (SOD) and myeloperoxidase (MPO). The pneumocyte apoptosis index (AI) was determined by terminal deoxynucleotidyl transferase mediated dUTP nick end labeling (TUNEL). Ultrastructural changes of lung tissue were observed by using transmission electron microscope. The results showed that in I/R group, the content of metallothionein was decreased (P<0.05), the content of MDA and MPO activity were increased (P<0.01), and SOD activity was decreased (P<0.01), compared with those in control group. IP treatment significantly increased the content of metallothionein (P<0.01), attenuated the MDA level (P<0.05) and MPO activity (P<0.01), and improved SOD activity (P<0.01) in blood serum. The number of TUNEL-positive cells in IP group was significantly reduced compared with that in I/R group (P<0.01). There were abnormal ultrastructural changes in I/R group, which were markedly reversed in IP group. In conclusion, IP may protect lung against I/R injury by inducing the expression of metallothionein.
