Long noncoding RNA X-inactive specific transcript (XIST) has been identified as a crucial regulator in neurodegenerative disorders. However, the role and mechanism of XIST in ischemic stroke remain elusive. In our study, we found that XIST expression was upregulated in both mice subjected to middle cerebral artery occlusion and oxygen-glucose deprivation (OGD)-treated neurons. Functional assays disclosed that the interference of XIST accelerated viability, and suppressed apoptosis and caspase-3 activity in OGD-treated neurons. Moreover, XIST interacted with miR-98, and miR-98 targeted BTB-to-CNC homology 1 (BACH1). miR-98 silencing or BACH1 overexpression counteracted XIST knockdown-mediated effects on cell viability and apoptosis in OGD-treated neurons. In conclusion, our data demonstrated that XIST facilitated the progression of ischemic stroke through regulating the miR-98/BACH1 axis. These findings might provide a novel therapeutic strategy for ischemic stroke treatment.

中文翻译：

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长链非编码 RNA X 失活特异性转录本通过 miR-98/BACH1 轴调节缺血性中风中的神经元细胞凋亡

长链非编码 RNA X 失活特异性转录本 (XIST) 已被确定为神经退行性疾病的关键调节因子。然而，XIST 在缺血性卒中中的作用和机制仍然难以捉摸。在我们的研究中，我们发现 XIST 表达在大脑中动脉闭塞和氧糖剥夺 (OGD) 处理的神经元的两只小鼠中上调。功能分析表明，XIST 的干扰加速了 OGD 处理神经元的活力，并抑制了细胞凋亡和 caspase-3 活性。此外，XIST 与 miR-98 相互作用，miR-98 靶向 BTB-to-CNC 同源 1 (BACH1)。miR-98 沉默或 BACH1 过表达抵消了 XIST 敲低介导的对 OGD 处理神经元细胞活力和细胞凋亡的影响。综上所述，我们的数据表明 XIST 通过调节 miR-98/BACH1 轴促进缺血性卒中的进展。这些发现可能为缺血性卒中治疗提供一种新的治疗策略。