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High fat-induced inflammation in vascular endothelium can be improved by Abelmoschus esculentus and metformin via increasing the expressions of miR-146a and miR-155

机译:Abelmoschus Esculentus和Metformin通过增加MiR-146a和miR-155的表达可以改善高脂肪诱导的血管内皮炎症

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Obesity is associated with chronic inflammation, which contributes to cardiovascular diseases. MicroRNAs (miRNAs) are reported to be involved in vascular inflammation and atherosclerosis. Abelmoschus esculentus (AE) and metformin have been suggested to improve inflammation in vascular system. The aim of this study is to evaluate whether miRNAs are involved in high fat induced endothelial inflammation, and whether AE and metformin improve endothelial inflammation by regulating miRNAs. We established high fat treated rats and human aortic endothelial cells (HAECs). AE and metformin were added to explore their effects on endothelial inflammation induced by high fat and the possible mechanism. The vascular inflammatory genes were increased in rats treated with high fat diet. The decreased miR-146a and miR-155 were involved in endothelial inflammation induced by high fat through targeting IL-1 receptor-associated kinase 1 (IRAK1), TNF receptor-associated factor 6 (TRAF6) and nuclear factor-κB p65 (NF-κB p65), respectively. While AE and metformin could ameliorate the endothelial inflammation by increasing miR-146a and miR-155. These results indicate that miR-146a and miR-155 play roles in the high fat induced endothelial inflammation, which could be potential therapeutic targets. AE and metformin can attenuate endothelial inflammation through regulating miR-146a and miR-155.
机译:肥胖与慢性炎症有关,有助于心血管疾病。据报道,MicroRNAs(miRNA)参与血管炎症和动脉粥样硬化。已经提出Abelmoschus esculentus(Ae)和二甲双胍来改善血管系统中的炎症。本研究的目的是评估miRNA是否参与高脂肪诱导的内皮炎症,以及是否通过调节miRNA来改善内皮炎。我们建立了高脂肪治疗的大鼠和人主动脉内皮细胞(HAECs)。加入AE和二甲双胍以探讨其对高脂肪诱导的内皮炎症的影响和可能的机制。高脂饮食处理的大鼠血管炎症基因增加。通过靶向IL-1受体相关激酶1(IRAK1),TNF受体相关因子6(TRAF6)和核因子-κBP65(NF-)涉及高脂肪诱导的内皮炎症诱导的内皮炎症涉及高脂肪诱导的内皮炎症(NF-分别为κBp65)。虽然AE和二甲双胍可以通过增加miR-146a和miR-155来改善内皮炎症。这些结果表明MIR-146A和MIR-155在高脂肪诱导的内皮炎症中发挥作用,这可能是潜在的治疗靶标。 AE和二甲双胍可以通过调节miR-146a和miR-155来衰减内皮炎症。

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