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作为apelin家族成员的apelin-36对离体大鼠心脏的影响。

The impact of apelin-36 on isolated rat hearts as a member of apelin family.

作者信息

Kutlay O

出版信息

Bratisl Lek Listy. 2018;119(10):625-629. doi: 10.4149/BLL_2018_111.

DOI:10.4149/BLL_2018_111
PMID:30345769
Abstract

BACKGROUND

Apelin is an endogenous adipocytokine that plays an important role in the regulation of cardiovascular function. Apelin-36 is a member of apelin family. However cardiac reports related to apelin-36 are very rare. The purpose of this study is to investigate the impact of apelin-36 on hemodynamic variables of the isolated rat hearts.

METHODS

Twenty-eight rats were equally divided into four groups: control, apelin-36 at the following concentrations: 1 nM, 10 nM and 100 nM. The isolated hearts were perfused with modified Krebs-Henseleit solution (mK-Hs) by using the Langendorff method. Cardiac parameters, including left ventricular developed pressure (LVDP), maximal rate of pressure development (+dP/dtmax), heart rate (HR) and coronary flow (CF) were measured. Gene expressions relevant to cardiomyocyte contractility were determined by real-time PCR.

RESULTS

10 and 100 nM doses of apelin-36 perfusion led to positive inotropy with an increase of LVDP and +dP/dtmax, which are the indexes of cardiac contractility. Furthermore both doses of apelin-36 increased endothelial nitric oxide synthase (eNOS), sarco/endoplasmic reticulum Ca2+-ATPase (Serca2a) and β2-Adrenergic receptors (β2-AR) mRNA.

CONCLUSION

These results showed that apelin-36 had a positive inotropic effect on the isolated rat heart and can induce eNOS, Serca2a and β2-AR genes activation that enhances contractility of the heart (Tab. 1, Fig. 2, Ref. 23).

摘要

背景

Apelin是一种内源性脂肪细胞因子,在心血管功能调节中起重要作用。Apelin-36是Apelin家族的成员。然而,与Apelin-36相关的心脏研究报告非常罕见。本研究的目的是探讨Apelin-36对离体大鼠心脏血流动力学变量的影响。

方法

28只大鼠平均分为四组:对照组、1 nM、10 nM和100 nM浓度的Apelin-36组。采用Langendorff法用改良的Krebs-Henseleit溶液(mK-Hs)灌注离体心脏。测量心脏参数,包括左心室舒张末压(LVDP)、最大压力上升速率(+dP/dtmax)、心率(HR)和冠状动脉血流量(CF)。通过实时PCR测定与心肌细胞收缩性相关的基因表达。

结果

10 nM和100 nM剂量的Apelin-36灌注导致正性肌力作用,LVDP和+dP/dtmax增加,这是心脏收缩性的指标。此外,两种剂量的Apelin-36均增加了内皮型一氧化氮合酶(eNOS)、肌浆网/内质网Ca2+-ATP酶(Serca2a)和β2-肾上腺素能受体(β2-AR)的mRNA。

结论

这些结果表明,Apelin-36对离体大鼠心脏具有正性肌力作用,并可诱导eNOS、Serca2a和β2-AR基因激活,增强心脏收缩力(表1,图2,参考文献23)。

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