首页> 外文期刊>Cellular & molecular biology letters. >Protective effect of intermedin on myocardial cell in a rat model of severe acute pancreatitis.
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Protective effect of intermedin on myocardial cell in a rat model of severe acute pancreatitis.

机译:Intermedin对重症急性胰腺炎大鼠模型心肌细胞的保护作用。

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Severe acute pancreatitis (SAP) is a common disease with a poor prognosis. Heart failure is one cause of SAP patient death. Intermedin (IMD) is a potent endogenous cardio-protective substance. Administration of exogenous IMD showed beneficial effects in cardiovascular diseases. The aim of this study was to investigate the myocardial damage in SAP and to determine the therapeutic potential of IMD for SAP. Using an SAP rat model, we examined endogenous IMD expression following SAP induction, and determined the effect of IMD on myocardial function, histological morphology, apoptosis-related gene expression, and prognosis. Our results indicated that the cardiac function and histological structure were significantly disrupted in SAP rats. Infusion of exogenous IMD significantly preserved cardiac function and ameliorated myocardial damage. Terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) revealed that myocardial apoptosis was extensively present in SAP rats, and IMD infusion led to increased expression of the prosurvival factor Bcl-2, but decreased pro-apoptotic factors Bax and caspase-3. In addition, IMD infusion also reversed the change of IMD receptor systems in SAP rat heart tissue. Furthermore, we found that IMD infusion greatly decreased mortality of SAP rats. In conclusion, administration of SAP produced therapeutic effects in SAP through modulating apoptotic and pro-survival gene expression, inhibiting myocardial apoptosis, preserving cardiac function, and a useful therapeutic agent for SAP, and provides us an insight for a clinical trial of IMD for treating human severe acute pancreatitis.
机译:重症急性胰腺炎(SAP)是一种预后较差的常见疾病。心力衰竭是SAP患者死亡的原因之一。 Intermedin(IMD)是有效的内源性心脏保护物质。外源IMD的施用显示出对心血管疾病的有益作用。这项研究的目的是调查SAP中的心肌损伤,并确定IMD对SAP的治疗潜力。使用SAP大鼠模型,我们检查了SAP诱导后内源性IMD的表达,并确定了IMD对心肌功能,组织形态,凋亡相关基因表达和预后的影响。我们的结果表明,SAP大鼠的心脏功能和组织学结构明显受损。输注外源IMD可显着保留心脏功能并减轻心肌损伤。末端脱氧核苷酸转移酶介导的dUTP缺口末端标记(TUNEL)显示,SAP大鼠中广泛存在心肌细胞凋亡,IMD注入导致生存因子Bcl-2的表达增加,但促凋亡因子Bax和caspase-3减少。此外,IMD输注还可以逆转SAP大鼠心脏组织中IMD受体系统的变化。此外,我们发现IMD输注大大降低了SAP大鼠的死亡率。总之,SAP的管理通过调节细胞凋亡和生存基因的表达,抑制心肌细胞凋亡,保留心脏功能以及对SAP有用的治疗剂,在SAP中产生了治疗效果,并为IMD的临床治疗提供了见识人类严重急性胰腺炎。

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