Endogenous ghrelin increases in adriamycin-induced heart failure rats.
Evidence has indicated that plasma ghrelin was elevated in chronic heart failure (CHF) patients with cachexia. The present report studied whether pathophysiologic increment of endogenous ghrelin levels was existed in the progression of adriamycin (ADR)-induced CHF, then the possible compensatory mechanism by which the changes were induced and the relationship between active ghrelin, cardiac function and energy reserve in heart failure (HF) rats were explored. Cardiac function, high energy phosphates (HEP) content, and ghrelin levels in plasma and myocardium were measured at 4 days, 1, 2 and 3 weeks after the last injection of ADR, after which correlation analysis was performed between these markers in HF rats. Results showed that cardiac function decreased early, then was significantly restored and worsened at 3 weeks accompanied by the decrease of myocardial ATP content. Plasma ghrelin level increased significantly at each time point while myocardial ghrelin level increased transiently, then was restored followed by increased oxidative stress status and apoptosis in the weakening heart. Moreover, correlation analysis indicated that the markers of cardiac function and HEP were positively correlated to the endogenous ghrelin levels at the HF stage. This study indicated that the increase of endogenous ghrelin levels during the progression of the HF induced by ADR represent a compensatory self-protective effect by improving cardiac function and retaining myocardial energy reserve; this may be closely linked to anti-oxidative and anti-apoptosis mechanisms through regulating myocardial mitochondria function by ghrelin; but further investigations are necessary.
Xu
Z
Z
Department of Pathophysiology, ZhongShan Medical College, Sun Yat-sen University, 74 Zhongshan Second Road, Guangzhou 510089, PR China.
Wu
W
W
Zhang
X
X
Liu
G
G
D000818:Animals; D018450:Disease Progression; D004317:Doxorubicin / Q000633:toxicity*; D054439:Ghrelin; D006333:Heart Failure / Q000097:blood / Q000139:chemically induced* / Q000378:metabolism*; D008297:Male; D009206:Myocardium / Q000378:metabolism; D036361:Peptide Hormones / Q000096:biosynthesis* / Q000097:blood / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar
D054439:Ghrelin; D036361:Peptide Hormones; D004317:Doxorubicin