Dysregulation of microRNAs (miRNAs) is involved in abnormal development and pathophysiology in the brain. Although miR-20b plays essential roles in various human diseases, its function in cerebral ischemic stroke remains unclear. A cell model of oxygen glucose deprivation/reoxygenation (OGD/R) and A rat model of middle cerebral artery occlusion/reperfusion (MCAO/R) were constructed. qRT-PCR and western blot were used to evaluate the expression of miR-20b and TXNIP. Cell viability was detected by MTT assay, and cell apoptosis was evaluated by flow cytometry. Targetscan and Starbase were used to predict the potential targets of miR-20b. Luciferase reporter assay was applied to determine the interaction between miR-20b and TXNIP. Rescue experiments were conducted to confirm the functions of miR-20b/TXNIP axis in cerebral ischemic stroke. MiR-20b was significantly downregulated after I/R both in vitro and in vivo. Upregulation of miR-20b inhibited OGD/R-induced neurons apoptosis and attenuated ischemic brain injury in rat model. Bioinformatic prediction suggested that TXNIP might be a target of miR-20b, and luciferase reporter assay revealed that miR-20b negatively regulated TXNIP expression by directly binding to the 3'-UTR of TXNIP. Downregulation of TXNIP inhibited OGD/R-induced neurons apoptosis in vitro and ischemic brain injury in vivo. Rescue experiments indicated that downregulation of TXNIP effectively reversed the effect of miR-20b inhibitor in neurons apoptosis after OGD/R-treatment and ischemic brain injury in a mouse model after MCAO/R-treatment. Our study demonstrated that upregulation of miR-20b protected the brain from ischemic brain injury by targeting TXNIP, extending our understanding of miRNAs in cerebral ischemic stroke.

中文翻译：

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通过靶向硫氧还蛋白相互作用蛋白（TXNIP），miR-20b的上调可预防脑缺血性中风。

microRNA（miRNA）的失调与大脑的异常发育和病理生理有关。尽管miR-20b在各种人类疾病中起着至关重要的作用，但其在脑缺血性中风中的功能仍不清楚。建立了氧葡萄糖剥夺/复氧的细胞模型（OGD / R）和大脑中动脉闭塞/再灌注的大鼠模型（MCAO / R）。采用qRT-PCR和western blot检测miR-20b和TXNIP的表达。通过MTT分析检测细胞活力，并通过流式细胞术评估细胞凋亡。Targetscan和Starbase用于预测miR-20b的潜在靶标。应用萤光素酶报告基因测定来确定miR-20b与TXNIP之间的相互作用。进行了抢救实验，以确认miR-20b / TXNIP轴在脑缺血性中风中的功能。体外和体内。在大鼠模型中，miR-20b的上调抑制了OGD / R诱导的神经元凋亡并减轻了缺血性脑损伤。生物信息学预测表明TXNIP可能是miR-20b的靶标，萤光素酶报告基因检测表明miR-20b通过直接结合TXNIP的3'-UTR负调节TXNIP的表达。TXNIP的下调抑制OGD / R诱导的神经元凋亡的体外和缺血性脑损伤的体内。救援实验表明，TXNIP的下调有效逆转了miR-20b抑制剂对OGD / R治疗后的神经元凋亡和MCAO / R治疗后的小鼠缺血性脑损伤的影响。我们的研究表明，miR-20b的上调通过靶向TXNIP保护大脑免受缺血性脑损伤的影响，从而扩展了我们对脑缺血性中风中miRNA的了解。