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首页> 外文期刊>Cellular Physiology and Biochemistry >MicroRNA-374 Exerts Protective Effects by Inhibiting SP1 Through Activating the PI3K/Akt Pathway in Rat Models of Myocardial Ischemia-Reperfusion After Sevoflurane Preconditioning
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MicroRNA-374 Exerts Protective Effects by Inhibiting SP1 Through Activating the PI3K/Akt Pathway in Rat Models of Myocardial Ischemia-Reperfusion After Sevoflurane Preconditioning

机译：MicroRNA-374在七氟醚预处理后的心肌缺血再灌注大鼠模型中通过激活PI3K / Akt途径抑制SP1发挥保护作用

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Background/Aims Ischemic heart disease is a leading cause of death in cardiovascular diseases, and microRNAs (miRs) have been reported to be potential therapeutic targets in heart disease. Herein, this study aims to investigate the effects of microRNA (miR)-374 on myocardial ischemia-reperfusion (I/R) injury in rat models pretreated with sevoflurane by targeting SP1 through the PI3K/Akt pathway. Methods SD rats were grouped into sham, I/R and sevoflurane + I/R (sevoflurane preconditioning and I/R) groups. The biochemical indicators, pathological changes, positive expression of SP1 protein, and apoptosis rates were measured using biochemical detection, Evans blue-TTC staining, immunohistochemistry and TUNEL staining. RT-qPCR and Western blotting were used to investigate the expression of miR-374 mRNA and the protein expression of SP1, PI3K, HO-1, p53, iNOS, c-fos, Akt/p-Akt, and GSK-3β/p-GSK-3β. Cardiomyocytes were treated with miR-374 mimics, miR-374 inhibitors, or siRNA-SP1. Cardiomyocyte proliferation and cycle distribution and apoptosis were studied by MTT and flow cytometry. Results Compared with the I/R group, in the sevoflurane + I/R group, serum SOD and IL-10 increased, while MDA, LDH, CK, TNF-α, IL-6 and IL-10 decreased, as did the percentage of infarct area, the positive rate of SP1 and the apoptosis index. The expression of SP1, p53, iNOS and c-fos decreased, and the miR-374 expression of PI3K, HO-1, Akt/p-Akt, GSK-3β/p-GSK-3β increased. With the upregulation of miR-374 and the downregulation of SP1, the expression of SP1, p53, iNOS and c-fos decreased, as did the proportion of cells in G1 phase and the apoptosis rate; the expression of PI3K, HO-1, Akt/p-Akt, GSK-3β/p-GSK-3β increased. The results in the miR-374 inhibitor group contrasted with the above results. Conclusion The results indicated that miR-374 could alleviate myocardial I/R damage in rat models pretreated with sevoflurane by targeting SP1 by activating the PI3K/Akt pathway.
机译：背景/目的缺血性心脏病是心血管疾病死亡的主要原因，据报道，microRNA（miRs）是心脏病的潜在治疗靶标。在本文中，本研究旨在通过通过PI3K / Akt途径靶向SP1，研究七氟醚预处理的大鼠模型中microRNA（miR）-374对心肌缺血/再灌注（I / R）损伤的影响。方法将SD大鼠分为假手术，I / R和七氟醚+ I / R（七氟醚预处理和I / R）组。使用生化检测，Evans blue-TTC染色，免疫组织化学和TUNEL染色来测量生化指标，病理变化，SP1蛋白阳性表达和凋亡率。用RT-qPCR和Western blotting检测miR-374 mRNA的表达以及SP1，PI3K，HO-1，p53，iNOS，c-fos，Akt / p-Akt和GSK-3β/ p的蛋白表达-GSK-3β。用miR-374模拟物，miR-374抑制剂或siRNA-SP1处理心肌细胞。用MTT和流式细胞术研究心肌细胞的增殖，周期分布和凋亡。结果与七氟醚+ I / R组相比，七氟醚+ I / R组血清SOD和IL-10升高，MDA，LDH，CK，TNF-α，IL-6和IL-10降低，百分率降低。梗死面积，SP1阳性率和细胞凋亡指数。 SP1，p53，iNOS和c-fos的表达降低，而PI3K，HO-1，Akt / p-Akt，GSK-3β/p-GSK-3β的miR-374表达升高。随着miR-374的上调和SP1的下调，SP1，p53，iNOS和c-fos的表达降低，G1期的细胞比例和凋亡率也降低。 PI3K，HO-1，Akt / p-Akt，GSK-3β/p-GSK-3β的表达增加。 miR-374抑制剂组的结果与上述结果相反。结论结果表明，miR-374可以通过激活PI3K / Akt途径靶向SP1，减轻七氟醚预处理的大鼠心肌I / R损伤。

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