【摘 要】
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Objective Ghrelin, a gastric hormone, exerts cardio-protective function by increasing myocardial contractility and vasodilation.The previous studies have reported that angiotensin Ⅱ (Ang Ⅱ) production
【机 构】
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Department of cardiology,China-Japan Union Hospital,Jilin University,Changchun,China
【出 处】
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2013中国医师协会中西医结合医师大会
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Objective Ghrelin, a gastric hormone, exerts cardio-protective function by increasing myocardial contractility and vasodilation.The previous studies have reported that angiotensin Ⅱ (Ang Ⅱ) production increased in heart failure, which can induce cardiomyocyte apoptosis.In the present study, we investigated the effect of ghrelin on Ang Ⅱ-induced H9c2 cardiomyocyte apoptosis.Methods and Results The results showed that Ang Ⅱ inhibited H9c2 cell viability, which was blocked by ghrelin.By annexin V-propidium iodide dual staining and TUNEL analysis, we found that Ang Ⅱ induced H9c2 cell apoptosis, while co-incubation of ghrelin with Ang Ⅱ significantly reduced H9c2 cell apoptosis induced by Ang Ⅱ.Simultaneously, the results revealed that ghrelin regulated the Ang Ⅱ-induced imbalance of Bax and Bcl-2 expression and reduced Ang Ⅱ-induced caspase-3 expression.Moreover, mRNA expressions of endoplasmic reticulum stress-related molecules GRP78, caspase-12 and CHOP were significantly upregulated by Ang Ⅱ.However, their expressions were significantly inhibited by ghrelin.In addition, we found that ghrelin markedly inhibited Ang Ⅱ-induced AT1 receptor expression.Conclusion These data suggest that ghrelin may play an antagonistic role in Ang Ⅱ-induced cardiomyocyte apoptosis via decreasing AT1 receptor expression and inhibiting activation of endoplasmic reticulum stress pathway.
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