Changes of leptin levels in serum and myocardium after myocardial ischemia/reperfusion injury.
- Author:
Hui XUE
1
;
Guang-tao YAN
;
Ji LIN
;
Xiu-hua HAO
;
Kai ZHANG
Author Information
- Publication Type:Journal Article
- MeSH: Animals; L-Lactate Dehydrogenase; metabolism; Leptin; blood; metabolism; Male; Myocardial Reperfusion Injury; metabolism; physiopathology; Myocardium; metabolism; Random Allocation; Rats; Rats, Sprague-Dawley
- From: Chinese Journal of Applied Physiology 2009;25(2):221-223
- CountryChina
- Language:Chinese
-
Abstract:
AIMTo explore the effect of rat myocardial ischemia/reperfusion injury on leptin levels in serum and myocardium, and discuss the role of leptin in myocardial ischemia/reperfusion injury.
METHODSA myocardial ischemia/reperfusion injury model of rats was established, serum lactate dehydrogenase (LDH) and leptin levels were detected, and histopathological changes and leptin expressions in myocardium were investigated by hematoxylin-eosin staining and immunohistochemistry, respectively.
RESULTSSerum LDH of ischemia and reperfusion groups increased significantly (P < 0.05), suggesting the model was successfully established and a certain degree of local myocardial injury was induced. Serum leptin of ischemia group (6.34 +/- 2.49) ng/ml was significantly lower than control group (7.50 +/- 2.93 ng/ml, P <0.05). Leptin levels recovered gradually after reperfusion, reached (8.32 +/- 1.74)ng/ml at 2 h after reperfusion, which recovered to the level before injury (8.38 +/- 2.56) ng/ml, and showed a trend to increase as reperfusion time was elongated. Immunohistochemistry results showed that as compared with sham-operation group, myocardial leptin protein expressions of the other four groups were all significantly lower (P < 0.01), and decreased in order by 45 min ischemia/1 h reperfusion, 45 min ischemia/3 h reperfusion, 45 min ischemia and 45 min ischemia/2 h reperfusion.
CONCLUSIONLeptin level in the blood decreases significantly at the early 45 min after myocardial ischemia/reperfusion injury, and its expression in myocardium also decreases significantly. There may be a certain relationship between the pathological injury of myocardium and the changes of leptin.