首页> 外文期刊>Revista da Associao Médica Brasileira >Vitamin D status influences cytokine production and MALAT1 expression from the PBMCs of patients with coronary artery disease and healthy controls
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Vitamin D status influences cytokine production and MALAT1 expression from the PBMCs of patients with coronary artery disease and healthy controls

机译:维生素D状态影响冠心病患者PBMC的细胞因子生产和MALAT1表达及健康对照

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OBJECTIVE: This study aimed to investigate the long non-coding RNA metastasis-associated lung adenocarcinoma transcript 1 (lncRNA MALAT1) expression and its role in cytokine production from peripheral blood mononuclear cells (PBMCs) in patients with coronary artery disease (CAD) and non-CAD participants (NCAD). METHODS: Blood samples were taken from 15 patients with CAD and 15 NCAD individuals. The plasma was used for biochemical analyses. MALAT1 and CD36 expressions were evaluated in the isolated peripheral blood mononuclear cells (PBMCs) by real-time PCR. Furthermore, the levels of inflammatory cytokines e.g. interleukin (IL)-6, IL-10, and IL-22 were measured in the supernatants of the cultured PBMCs by flow cytometry. RESULTS: The levels of MALAT1 and CD36 were not significantly different between the CAD and NCAD groups. However, a lower level of MALAT1 and CD36 was observed in PBMCs of vitamin D deficient (15 ng/ml) CAD and NCAD participants. Furthermore, the vitamin D deficient (15 ng/ml) group showed a significantly higher plasma level of IL-6, IL-10, and IL-22 compared to the non-deficient (≥15 ng/ml) group. In addition, significant positive correlations were found between CD36, IL-22, and fasting blood sugar (FBS) with MALAT1. CONCLUSION: Given that in vitamin D deficient individuals a decreased level of MALAT1 was associated with CD36 expression and increased IL-22 production, vitamin D supplementation may play a role in reducing MALAT1/CD36/IL-22 mediated complications such as T2DM and CAD, especially in vitamin D deficiency.
机译:目的:本研究旨在探讨长期非编码RNA转移相关肺腺癌转录1(LNCRNA MALAT1)表达及其在冠状动脉疾病(CAD)和非患者外周血单核细胞(PBMC)中的细胞因子生产中的作用。 -CAD参与者(NCAD)。方法:采用15例CAD和15个NCAD个体血液样品。血浆用于生物化学分析。通过实时PCR在分离的外周血单核细胞(PBMC)中评估Malat1和CD36表达。此外,炎症细胞因子的水平例如。通过流式细胞术在培养的PBMC的上清液中测量白细胞介素(IL)-6,IL-10和IL-22。结果:CAD和NCAD组之间MALAT1和CD36的水平没有显着差异。然而,在维生素D缺乏(<15ng / mL)CAD和NCAD参与者的PBMC中观察到较低水平的MALAT1和CD36。此外,与非缺陷(≥15ng/ ml)组相比,维生素D缺陷(<15 ng / ml)组显示出IL-6,IL-10和IL-22的显着更高的血浆水平。此外,CD36,IL-22和用MALAT1的空腹血糖(FBS)之间发现了显着的正相关性。结论:鉴于维生素D缺乏个体,MALAT1的降低与CD36表达和IL-22产生的增加,维生素D补充可能在减少MALAT1 / CD36 / IL-22介导的并发症等中,如T2DM和CAD的作用。特别是在维生素D缺乏。

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