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首页> 外文期刊>Life sciences >Arginine vasopressin increases iNOS-NO system activity in cardiac fibroblasts through NF-kappaB activation and its relation with myocardial fibrosis.
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Arginine vasopressin increases iNOS-NO system activity in cardiac fibroblasts through NF-kappaB activation and its relation with myocardial fibrosis.

机译：精氨酸加压素通过NF-κB活化及其与心肌纤维化的关系增加心脏成纤维细胞中iNOS-NO系统的活性。

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Previous studies have shown that arginine vasopressin (AVP) promotes myocardial fibrosis (MF), whereas nitric oxide (NO) inhibits MF. Cardiac fibroblasts (CFs) are the main target cells of MF. However, the modulatory effect of AVP on NO production in CFs and the role of this effect in MF are still unknown. In the present study, CFs obtained from Sprague-Dawley rats were stimulated with or without AVP and pyrrolidine dithiocarbamate (PDTC), a specific inhibitor of nuclear factor kappa-B (NF-kappaB). NO production and NOS activity were detected with absorption spectrometry, inducible nitric oxide synthase (iNOS) protein with Western blot analysis, iNOS mRNA with real-time PCR, CF collagen synthesis with [(3)H]proline incorporation, and NF-kappaB activation with immunofluorescence staining and Western blot analysis. The results showed that AVP increased NO production in a dose- and time-dependent manner, with maximal effects at 10(-7) mol/l after 24-h stimulation. AVP also increased NOS activity, protein and mRNA levels of iNOS in a coincident manner. Furthermore, AVP also increased CF collagen synthesis in a dose- and time-dependent manner. In addition, it was found that NF-kappaB was activated by AVP, and that PDTC could inhibit NO production, NOS activity, protein and mRNA levels of iNOS stimulated by AVP in a dose-dependent manner. The inhibitory effects of PDTC on NF-kappaB translocation were coincident with the effects of PDTC on iNOS-NO system activity. It is suggested that AVP increases NO production via the regulation of iNOS gene expression, and the upregulation of iNOS gene expression stimulated by AVP is mediated through NF-kappaB activation. NO production induced by AVP may counteract the profibrotic effects of AVP, thus the development of MF perhaps depends on the balance between profibrotic AVP and antifibrotic NO effects on MF.
机译：先前的研究表明，精氨酸加压素（AVP）促进心肌纤维化（MF），而一氧化氮（NO）抑制MF。心脏成纤维细胞（CFs）是MF的主要靶细胞。然而，AVP对CFs中NO产生的调节作用及其在MF中的作用仍然未知。在本研究中，从Sprague-Dawley大鼠获得的CFs在有或没有AVP和吡咯烷二硫代氨基甲酸酯（PDTC）（一种核因子kappa-B（NF-kappaB）的特异性抑制剂）的刺激下进行。用吸收光谱法检测NO产生和NOS活性，用Western印迹分析检测诱导型一氧化氮合酶（iNOS）蛋白，用实时PCR检测iNOS mRNA，通过[（3）H]脯氨酸掺入CF胶原蛋白，并检测NF-κB活化免疫荧光染色和蛋白质印迹分析。结果表明，AVP以剂量和时间依赖的方式增加NO的产生，在刺激24小时后的最大效应为10（-7）mol / l。 AVP还以一致的方式增加了iNOS的NOS活性，蛋白质和mRNA水平。此外，AVP还以剂量和时间依赖性方式增加CF胶原蛋白的合成。此外，还发现NF-κB被AVP激活，PDTC可以剂量依赖性地抑制AVP刺激的iNOS的NO产生，NOS活性，蛋白质和mRNA水平。 PDTC对NF-κB易位的抑制作用与PDTC对iNOS-NO系统活性的影响相吻合。提示AVP通过调节iNOS基因表达增加NO的产生，而AVP刺激的iNOS基因表达的上调是通过NF-κB的激活介导的。 AVP诱导的NO产生可能抵消AVP的促纤维化作用，因此MF的发展可能取决于促纤维化AVP和抗MF对MF的平衡。

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