首页> 外文期刊>Balkan Medical Journal >The Effect of Chemerin on Cardiac Parameters and Gene Expressions in Isolated Perfused Rat Heart
【24h】

The Effect of Chemerin on Cardiac Parameters and Gene Expressions in Isolated Perfused Rat Heart

机译:凯莫瑞对离体灌注大鼠心脏心脏参数和基因表达的影响

获取原文
       

摘要

Background: Chemerin is a novel chemoattractant adipokine expressed in cardiovascular system, and its receptor has been detected in the epicardial adipose tissue. Aims: To determine the effects of chemerin on the cardiac parameters and gene expressions in the isolated perfused rat heart. Study Design: Animal experiment. Methods: The hearts were retrogradely perfused with Langendorff technique to measure the cardiac parameters. The experimental groups were acutely treated with 10, 100, and 1000 nM doses of chemerin. Another group was given 10 μM L-nitric oxide synthase inhibitor for 5 min before 1000 nM chemerin administration. The real-time polymerase chain reaction was performed for detecting the expression of target genes. Results: All doses of chemerin significantly decreased the left ventricular developed pressure (max 35.33 Δ%, p0.001), and +dP/dtsubmax/sub (max 31.3 Δ%, p0.001), which are the indexes of cardiac contractile force. In addition, 1000 nM chemerin reduced the coronary flow (max 31 Δ%, p0.001). N(W)-nitro-L-arginine methyl ester antagonized the negative inotropic effect of chemerin on contractility. Chemerin induced a 2.16-fold increase in endothelial nitric oxide synthase mRNA and increased the cyclic guanosine monophosphate levels (p0.001) but decreased the PI3Kγ gene expression (1.8-fold, p0.001). Furthermore, all doses of chemerin decreased the CaV1.2 gene expression (1.69-fold, p0.001). Conclusion: Acute chemerin treatment induces a negative inotropic action with the involvement of nitric oxide pathway, CaV1.2, and PI3Kγ on isolated rat heart.
机译:背景:Chemerin是一种在心血管系统中表达的新型趋化因子脂肪因子,其受体已在心外膜脂肪组织中被检测到。目的:确定凯莫瑞对离体灌注大鼠心脏的心脏参数和基因表达的影响。研究设计:动物实验。方法:用Langendorff技术逆行灌注心脏以测量心脏参数。实验组分别用10、100和1000 nM的凯莫瑞剂量进行了急性治疗。另一组在给予1000 nM凯莫瑞之前给予10μML一氧化氮合酶抑制剂5分钟。进行实时聚合酶链反应以检测靶基因的表达。结果:所有剂量的凯莫瑞均显着降低左心室发育压力(最大35.33Δ%,p <0.001)和+ dP / dt max (最大31.3Δ%,p <0.001),分别为心脏收缩力的指标。此外,1000 nM chemerin降低了冠状动脉血流量(最大31Δ%,p <0.001)。 N(W)-硝基-L-精氨酸甲酯拮抗凯莫瑞对收缩力的负性变力作用。凯莫瑞诱导内皮一氧化氮合酶mRNA增加2.16倍,并增加环鸟苷单磷酸水平(p <0.001),但降低PI3Kγ基因表达(1.8倍,p <0.001)。此外,所有剂量的凯莫瑞均降低CaV1.2基因的表达(1.69倍,p <0.001)。结论:急性凯莫瑞治疗可引起离体大鼠心脏负性肌力作用,其中一氧化氮途径,CaV1.2和PI3Kγ参与其中。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号