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首页> 外文期刊>Cellular Physiology and Biochemistry >Association Between C1q/TNF-Related Protein-1 Levels in Human Plasma and Epicardial Adipose Tissues and Congestive Heart Failure
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Association Between C1q/TNF-Related Protein-1 Levels in Human Plasma and Epicardial Adipose Tissues and Congestive Heart Failure

机译：人血浆和心外膜脂肪组织中C1q / TNF相关蛋白1水平与充血性心力衰竭之间的关联

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>Background/Aims: C1q and tumour necrosis factor-related protein 1 (CTRP1) possesses anti-atherogenic and anti-inflammatory effects. This study investigated whether the CTRP1 levels in the plasma and epicardial adipose tissue (EAT) were associated with congestive heart failure (CHF) and to disclose possible molecular mechanisms. Methods: Plasma and tissue samples were obtained from subjects with or without CHF. Plasma levels of CTRP1 were measured by ELISA. The mRNA levels of CTRP1 and inflammatory cytokines were detected by RT-PCR. The protein levels of CTRP1, aldosterone synthase (CYP11B2) and mitogen-activated protein kinase were examined by Western blotting. Results: The levels of CTRP1 in the plasma and EAT were higher in the CHF patients than those in the controls. There were no differences in the CTRP1 levels in cardiomyocytes between the CHF group and the non-CHF group. An exploratory survival analysis showed that higher CTRP1 values at admission were associated with a worse prognosis after discharge. CTRP1 increased the IL-6 mRNA level in H295R cells. CTRP1 recruited ERK1/2 and Jak-2 for aldosterone release by modulating the CYP11B2 protein level, and brain natriuretic peptide repressed the CTRP1-induced aldosterone release through the JAK2-STAT3 signalling pathways. Conclusion: The CTRP1 levels in the plasma and EAT were increased in the CHF patients. CTRP1 is involved in the pathogenesis of CHF by modulating IL-6 levels and aldosterone release.
机译：> 背景/目的： C1q和肿瘤坏死因子相关蛋白1（CTRP1）具有抗动脉粥样硬化和抗炎作用。这项研究调查了血浆和心外膜脂肪组织（EAT）中的CTRP1水平是否与充血性心力衰竭（CHF）相关，并揭示了可能的分子机制。 方法： 血浆和组织样品取自患有或未患有CHF的受试者。通过ELISA测量血浆CTRP1水平。通过RT-PCR检测CTRP1和炎症细胞因子的mRNA水平。通过蛋白质印迹法检测CTRP1，醛固酮合酶（CYP11B2）和丝裂原激活的蛋白激酶的蛋白水平。 结果： CHF患者血浆和EAT中的CTRP1水平高于对照组。 CHF组和非CHF组之间，心肌细胞的CTRP1水平没有差异。一项探索性生存分析表明，入院时较高的CTRP1值与出院后预后较差有关。 CTRP1增加了H295R细胞中IL-6 mRNA的水平。 CTRP1通过调节CYP11B2蛋白水平募集ERK1 / 2和Jak-2来释放醛固酮，而脑利钠肽通过JAK2-STAT3信号通路抑制CTRP1诱导的醛固酮释放。 结论： CHF患者血浆和EAT的CTRP1水平升高。 CTRP1通过调节IL-6水平和醛固酮释放而参与CHF的发病过程。

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