growth hormone secretagogues protect mouse cardiomyocytes from in vitro ischemiareperfusion injury through regulation of intracellular calcium生长激素促分泌素防止老鼠心肌细胞体外ischemiareperfusion损伤通过调节细胞内钙.pdfVIP

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growth hormone secretagogues protect mouse cardiomyocytes from in vitro ischemiareperfusion injury through regulation of intracellular calcium生长激素促分泌素防止老鼠心肌细胞体外ischemiareperfusion损伤通过调节细胞内钙.pdf

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growth hormone secretagogues protect mouse cardiomyocytes from in vitro ischemiareperfusion injury through regulation of intracellular calcium生长激素促分泌素防止老鼠心肌细胞体外ischemiareperfusion损伤通过调节细胞内钙

Growth Hormone Secretagogues Protect Mouse Cardiomyocytes from in vitro Ischemia/Reperfusion Injury through Regulation of Intracellular Calcium 1 2 1 1 1 Yi Ma , Lin Zhang , Joshua N. Edwards , Bradley S. Launikonis , Chen Chen * 1 School of Biomedical Sciences, University of Queensland, Brisbane, Queensland, Australia, 2 School of Biological Sciences, University of Auckland, Auckland, New Zealand Abstract Background: Ischemic heart disease is a leading cause of mortality. To study this disease, ischemia/reperfusion (I/R) models are widely used to mimic the process of transient blockage and subsequent recovery of cardiac coronary blood supply. We aimed to determine whether the presence of the growth hormone secretagogues, ghrelin and hexarelin, would protect/ improve the function of heart from I/R injury and to examine the underlying mechanisms. Methodology/Principal Findings: Isolated hearts from adult male mice underwent 20 min global ischemia and 30 min reperfusion using a Langendorff apparatus. Ghrelin (10 nM) or hexarelin (1 nM) was introduced into the perfusion system either 10 min before or after ischemia, termed pre- and post-treatments. In freshly isolated cardiomyocytes from these hearts, single cell shortening, intracellular calcium ([Ca2+] ) transients and caffeine-releasable sarcoplasmic reticulum (SR) i Ca2+ were measured. In addition, RT-PCR and Western blots were used to examine the expression level of GHS receptor type 1a (GHS-R1a), and phosphorylated phospholamban (p-PLB), respectively. Ghrelin and hexarelin pre- or post-treatments prevented the significant reduction in the cell shorte