首页> 外文期刊>European Journal of Pharmacology: An International Journal >Geniposide alleviates hypoxia-induced injury by down-regulation of lncRNA THRIL in rat cardiomyocytes derived H9c2 cells
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Geniposide alleviates hypoxia-induced injury by down-regulation of lncRNA THRIL in rat cardiomyocytes derived H9c2 cells

机译:Geniposide通过在大鼠心肌细胞衍生H9C2细胞的大鼠心肌细胞中,减轻缺氧诱导的损伤。

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摘要

Geniposide (GEN) is an iridoid glycoside extracts from Gardenia jasminoides Ellis with antioxidant and anti-inflammarory properties. The objective of this study was to explore the effects of GEN on a cell model of myocardial infarction (MI). After transfection, hypoxia-stimulated H9c2 cells were treated with GEN. Cell viability and apoptosis were detected by Cell Counting kit-8 assay and flow cytometry, respectively. Cell cycle-, apoptosis- and signal pathway related proteins were examined by Western blot. The expression of THRIL was determined by qRT-PCR. In addition, in vivo experiments were performed in rats. Then the infarct size and the left ventricular (LV) end diastolic diameter (LVEDD), LV ejection fraction (LVEF) and LV fractional shortening (LVFS) were monitored. Results showed that treating H9c2 cells with GEN attenuated hypoxia-induced cell damage as cell viability was increased, and cell apoptosis was repressed. Meanwhile, THRIL was found to be down-regulated by GEN. The cardioprotective effects of GEN on H9c2 cells were attenuated when THRIL was overexpressed. Besides this, the phosphorylation of PI3K, AKT, JAK1 and STAT3 were up-regulated by GEN while down-regulated by THRIL overexpression. Moreover, GEN decreased infarct size and LVEDD, while increased LVEF and LVFS. Taken together, this study demonstrated that GEN alleviated cardiomyocytes damage and cardiac dysfunction possible through down-regulation of THRIL.
机译:Geniposide(Gen)是一种来自Gardenia Jasminoides Ellis的伊里安苷醇提取物,具有抗氧化剂和抗炎性质。本研究的目的是探讨Gen对心肌梗死(MI)细胞模型的影响。转染后,用Gen处理缺氧刺激的H9C2细胞。通过细胞计数试剂盒-8测定和流式细胞术检测细胞活力和细胞凋亡。通过Western印迹检查细胞周期,凋亡和信号途径相关蛋白质。通过QRT-PCR测定三分的表达。此外,在体内实验中在大鼠进行。然后监测梗死尺寸和左心室(LV)末端舒张直径(LVED),LV喷射分数(LVEF)和LV分数缩短(LVFS)。结果表明,随着细胞活力的增加,将H9C2细胞与Gen测量的缺氧诱导的细胞损伤进行治疗,并将细胞凋亡抑制被抑制。同时,发现基因受到基因下调。当Thril过表达时,Gen在H9C2细胞上的心脏保护作用衰减。除此之外,PI3K,AKT,JAK1和STAT3的磷酸化由GEN调节,而基于过度表达抑制。此外,Gen降低了梗塞尺寸和LVEDD,而LVEF和LVFs增加。这项研究总结在一起,表明,Gen缓解了Chariomy细胞的损伤和心脏功能障碍,可以通过下调来调节。

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