Background: Hypoxic-ischaemic encephalopathy (HIE) is a prevailing severe brain damage disease in newborns, and caused by perinatal asphyxia cerebral ischaemia and reperfusion. Here, we investigated the role of cZNF292 in oxygen-glucose deprivation/reperfusion (OGD/R)-induced neural stem cells (NSCs) injury, and explored the underlying molecular mechanism.Methods: Before NSCs were subjected to OGD/R treatment, NSCs were transfected with or without overexpressing cZNF292, si-cZNF292 or miR-22 inhibitor. Viability, apoptosis and potential molecular mechanism were examined. Cell viability and apoptotic rate were evaluated utilizing cell counting kit-8 (CCK-8) and flow cytometry. The cZNF292 and miR-22 expression was determined utilizing quantitative reverse transcription-PCR (qRT-PCR). Moreover, apoptosis and Wnt/β-catenin and PKC/ERK pathways-associated proteins were quantified applying western blot.Results: OGD/R repressed viability and promoted apoptosis of NSCs. Also, cZNF292 expression was promoted by OGD/R treatment. Moreover, cZNF292 overexpression further caused OGD/R-stimulated damage. Inversely, silencing cZNF292 alleviated OGD/R-stimulated damage in NSCs. In addition, miR-22 expression was negatively regulated by cZNF292. It was confirmed that silencing cZNF292 attenuated OGD/R-induced NSCs injury and promoted the activation of Wnt/β-catenin and PKC/ERK pathways via the up-regulation of miR-22.Conclusions: The cZNF292 silence alleviated OGD/R-induced injury through the up-regulation of miR-22 in NSCs, and which furnished the theoretical basis for further research on HIE progression.

中文翻译：

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环状 RNA cZNF292 沉默通过上调大鼠神经干细胞 (NSC) 中的 miR-22 来减轻 OGD/R 诱导的损伤。

背景：缺氧缺血性脑病（HIE）是新生儿常见的严重脑损伤疾病，由围产期窒息性脑缺血再灌注引起。在这里，我们研究了 cZNF292 在氧-葡萄糖剥夺/再灌注 (OGD/R) 诱导的神经干细胞 (NSCs) 损伤中的作用，并探讨了潜在的分子机制。方法：在 NSCs 进行 OGD/R 治疗之前，NSCs在有或没有过表达 cZNF292、si-cZNF292 或 miR-22 抑制剂的情况下转染。检查了活力、细胞凋亡和潜在的分子机制。使用细胞计数试剂盒 8 (CCK-8) 和流式细胞术评估细胞活力和凋亡率。利用定量逆转录-PCR (qRT-PCR) 测定 cZNF292 和 miR-22 的表达。而且，应用western blot对细胞凋亡和Wnt/β-catenin和PKC/ERK通路相关蛋白进行定量。结果：OGD/R抑制NSCs的活力并促进NSCs的凋亡。此外，OGD/R 处理促进了 cZNF292 的表达。此外，cZNF292 过表达进一步引起 OGD/R 刺激的损伤。相反，沉默 cZNF292 减轻了 NSC 中 OGD/R 刺激的损伤。此外，miR-22 的表达受到 cZNF292 的负调控。证实沉默cZNF292可减轻OGD/R诱导的NSCs损伤，并通过上调miR-22促进Wnt/β-catenin和PKC/ERK通路的激活。结论：cZNF292沉默可减轻OGD/R诱导的神经干细胞损伤。通过上调 NSCs 中 miR-22 的损伤，为进一步研究 HIE 进展提供了理论基础。