Mechanism Of Ghrelin In Improving Cardiac Function By Inhibiting Endoplasmic Reticulum Stress In Rats With Acute Myocardial Infarction

Objective To establish the acute myocardial infarction (AMI) in rats,and to explore the mechanism of Ghrelin in improving cardiac functionthrough inhibiting endoplasmic reticulum stress (ERS).Methods AMI model was reproduced in18adult maleSprague-Dawley rats (220±20g) by ligation of the left anterior descendingcoronary artery. Four days after the reproduction of the model,14survivedrats with AMI were randomly divided into two groups (7each): model group,animals were subcutaneously (sc) injected with normal saline only;treatment group, animals were given Ghrelin (100μg/kg) twice a day (12hinterval) for two weeks. In addition, a sham-operated group was set up(Sham operation+saline, n=8). Two weeks later, the cardiac function wasexamined by echocardiography (UCG), the morphological changes inmyocardial tissue were observed by hematoxylin-eosin (HE) staining, thelevels of LDH and CK-MB were determined by ELISA, and the expressionsof glucose-regulated protein-78(GRP-78) and C/EBP homologous protein (CHOP) were assessed by Western blotting.Results AMI model was successfully reproduced in SD rats.Compared with the rats in sham group, those in model group showed poorcardiac function (P<0.05), HE staining revealed loosening of tissue andedema, ELISA revealed elevation of serum LDH and CK-MB levels(P<0.05), and up regulation of expressions of GRP-78and CHOP protein(P<0.05). While compared with model group, rats in treatment groupshowed better cardiac function (P<0.05), tissue loosening and edema werealleviated, the levels of serum LDH and CK-MB lowered (P<0.05), anddecreased the expressions of GRP-78and CHOP protein (P<0.05).Conclusion Ghrelin may improve the cardiac function by inhibitingERS, thus ameliorating the myocardial damage caused by AMI.