[Preliminary investigation of the changes and mechanism of Leptin after myocardial ischemia/reperfusion injury].

OBJECTIVE

To explore the effect of rat myocardial ischemia/reperfusion (I/R) injury on serum Leptin, endothelin (ET), C-reactive protein (CRP) and myocardial Leptin expression, and discuss the role of Leptin in myocardial I/R injury.

METHODS

Fifty Sprague-Dawley (SD) rats were randomly divided into sham-operation, ischemia and I/R 1, 2, 3 hours groups, with 10 rats in each group. Anterior descending artery of the left coronary artery was ligated for 45 minutes and released for 1, 2 and 3 hours to establish myocardial I/R model, and the said artery of the rats in sham-operation group was not ligated. Blood from left femoral artery was collected at different time points, and serum Leptin, ET and CRP contents were detected. Myocardial tissue was harvested, and stained with hematoxylin-eosin (HE) and immunohistochemistry for its observation of the myocardial pathological changes and Leptin protein expression.

RESULTS

Serum Leptin content (μg/L) of ischemia group was significantly lower than that of sham-operation group (4.69±1.67 vs. 6.48±2.02, P<0.05); as the reperfusion time was prolonged, serum Leptin level increased gradually, and the level of I/R 3-hour group recovered to that before injury [(6.59±2.58) μg/L]. ET content (ng/L) of ischemia group was significantly higher than that of sham-operation group (110.58±37.86 vs. 80.74±34.43, P<0.05), the levels of ET in I/R 1, 2 and 3 hours groups were significantly lower than those of ischemia group (35.87±13.56, 31.98±10.88, 34.56±14.37 vs. 110.58±37.86, all P<0.05). CRP content (mg/L) of ischemia group was significantly higher than that of sham-operation group (13.12±4.82 vs. 3.24±1.72, P<0.01); as the reperfusion time was prolonged, serum CRP level increased gradually, and the levels of I/R 1, 2 and 3 hours groups were significantly higher than those of ischemia group (18.37±6.48, 24.30±9.51, 27.08±8.32 vs. 13.12±4.82, all P<0.05). Pathological examination showed that there was necrosis of ischemic myocardial cells in ischemia group, with mild congestion and edema in interstitial spaces. After I/R injury, the myocardial cells showed coagulative necrosis, and there was severe congestion of myocardial interstitial. Immunohistochemistry results showed that there was a tendency of decrease in Leptin protein expression in the early phase but increase in the late phase after the injury.

CONCLUSION

Leptin content in the serum and myocardial tissue decreases significantly in the early phase after myocardial I/R but increases gradually in the rehabilitative phase, suggesting that Leptin maybe a stress protective factor against I/R-induced myocardial injury. There is a possible association between Leptin and the early increase followed by a delayed decrease of ET as well as the increase of CRP.