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Steroid receptor RNA activator affects the development of poststroke depression by regulating the peroxisome proliferator-activated receptor gamma signaling pathway

机译:类固醇受体RNA活化剂通过调节过氧化物酶促增殖物激活的受体γ信号传导途径来影响失败抑制的发育

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摘要

The long noncoding RNA, steroid receptor RNA activator (SRA), has been reported to be involved in the development of many types of disease in humans. The aim of this study was to evaluate whether SRA was associated with poststroke depression (PSD). A PSD rat model was established, and depression-like behaviors and sucrose consumption in rats with PSD were analyzed. Reverse transcription-quantitative PCR (RT-PCR), western blot and luciferase dual reporter assay analyses were performed to detect the expression of peroxisome proliferator-activated receptor. (PPAR.) expression following SRA small interfering RNA (siRNA) treatment. Compared with the control, the horizontal and vertical movement scores and consumption of sucrose solution were decreased in the PSD, PSD + LV-SRA and PSD + pioglitazone groups at 7 days post-SRA-siRNA treatment, while they were increased in the PSD + LV-SRA and PSD + pioglitazone groups. Furthermore, SRA expression in the PSD, PSD + LV-SRA and PSD + pioglitazone groups was lowered compared with the control group at 7 days postinjection. SRA increased the reported luciferase activity, but pioglitazone had no effect on the luciferase activity induced by SRA. SRA upregulated PPAR. mRNA and protein expression, whereas SRA siRNA significantly downregulated its expression. No significant differences in characteristics were identified between rats with and without PSD. SRA was more highly expressed in rats with PSD than rats without PSD. Collectively, this study suggests that SRA is associated with PSD through PPAR. signaling, indicating a potential therapeutic target of SRA for controlling PSD. NeuroReport 31: 48-56 Copyright (c) 2019 The Author(s). Published by Wolters Kluwer Health, Inc.
机译:据报道,长期的非编码RNA,类固醇受体RNA活化剂(SRA)参与人体中许多类型的疾病的发展。本研究的目的是评估SRA是否与卒中后抑郁(PSD)有关。建立了PSD大鼠模型,分析了PSD大鼠的抑郁类行为和蔗糖消耗。进行逆转录定量PCR(RT-PCR),进行蛋白质印迹和荧光素酶双报告分析分析以检测过氧化物体增殖物激活受体的表达。 (PPAR。)表达后SRA小干扰RNA(siRNA)治疗。与对照相比,在SRA-siRNA治疗后7天,PSD,PSD + LV-SRA和PSD + Pioglitazone基团的水平和垂直运动分数和蔗糖溶液的消耗量降低,同时在PSD +中增加它们LV-SRA和PSD + Pioglitazone组。此外,与对照组的PSD,PSD + LV-SRA和PSD + Pioglitazone基团的SRA表达降低,与对照组在发射后7天突出。 SRA增加了报告的荧光素酶活性,但吡格列酮对SRA诱导的荧光素酶活性没有影响。 SRA上调PPAR。 mRNA和蛋白质表达,而SRA siRNA显着下调其表达。在具有和没有PSD的大鼠之间鉴定了特征的显着差异。在没有PSD的大鼠的大鼠中,SRA比没有PSD的大鼠更高度表达。集体,该研究表明,SRA通过PPAR与PSD相关联。信号传导,表明SRA的潜在治疗目标用于控制PSD。 NeurorePort 31:48-56 2019年版权所有(C)。由Wolters Kluwer Health,Inc。出版

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