Hypoxic-ischemic encephalopathy (HIE) is a detrimental factor in infant death and chronic disease. The specific pathogenesis is not entirely clear. Therefore, exploring the pathogenesis of HIE is critical. The expression of miR-19b-3p and SOX6 in umbilical blood of HIE patients was detected by qRT-PCR assay. HT22 cells were triggered with oxygen-glucose deprivation/reoxygenation (OGD/R) to construct the HIE cell model. Cell Counting Kit-8 (CCK-8) assay was used to estimate viability. SOD and MDA levels were detected by enzyme linked immunosorbent assay. Flow cytometry was implemented to ascertain neurocyte apoptosis. Cellular β-catenin immunofluorescence staining was used to detect the expression and distribution of β-catenin protein. Wnt signaling pathway activation was detected by TOPFlash/FOPFlash luciferase reporter assay. The targeting correlation of SOX6 and miR-19b-3p was corroborated by dual-luciferase reporter gene assay and RNA pull-down assay. MiR-19b-3p expression was once down-regulated, whilst SOX6 expression was up-regulated in HIE patients. MiR-19b-3p overexpression promoted cell proliferation, repressed cell apoptosis, oxidative stress response, and Wnt/β-catenin pathway activation in OGD/R-triggered HT22 cells. MiR-19b-3p negatively regulated SOX6 expression. SOX6 knockdown improved OGD/R-triggered HT22 cells injury via Wnt/β-catenin pathway activation. MiR-19b-3p overexpression suppressed OGD/R-triggered HT22 cell injury via inhibiting SOX6 expression via activating Wnt/β-catenin pathway.

缺氧缺血性脑病 (HIE) 是婴儿死亡和慢性疾病的有害因素。具体发病机制尚不完全清楚。因此，探索HIE的发病机制至关重要。采用qRT-PCR法检测HIE患者脐血中miR-19b-3p和SOX6的表达。HT22 细胞被氧-葡萄糖剥夺/复氧 (OGD/R) 触发以构建 HIE 细胞模型。细胞计数 Kit-8 (CCK-8) 测定用于估计生存力。SOD和MDA水平通过酶联免疫吸附试验检测。实施流式细胞术以确定神经细胞凋亡。采用细胞β-catenin免疫荧光染色检测β-catenin蛋白的表达和分布。Wnt 信号通路激活通过 TOPFlash/FOPFlash 荧光素酶报告基因检测进行检测。双荧光素酶报告基因测定和 RNA pull-down 测定证实了 SOX6 和 miR-19b-3p 的靶向相关性。MiR-19b-3p 表达一度下调，而 SOX6 表达在 HIE 患者中上调。在 OGD/R 触发的 HT22 细胞中，MiR-19b-3p 过表达促进细胞增殖、抑制细胞凋亡、氧化应激反应和 Wnt/β-catenin 通路激活。MiR-19b-3p 负向调节 SOX6 表达。SOX6 敲低通过 Wnt/β-catenin 通路激活改善了 OGD/R 触发的 HT22 细胞损伤。MiR-19b-3p 过表达通过激活 Wnt/β-catenin 通路抑制 SOX6 表达，从而抑制 OGD/R 触发的 HT22 细胞损伤。而 SOX6 表达在 HIE 患者中上调。在 OGD/R 触发的 HT22 细胞中，MiR-19b-3p 过表达促进细胞增殖、抑制细胞凋亡、氧化应激反应和 Wnt/β-catenin 通路激活。MiR-19b-3p 负向调节 SOX6 表达。SOX6 敲低通过 Wnt/β-catenin 通路激活改善了 OGD/R 触发的 HT22 细胞损伤。MiR-19b-3p 过表达通过激活 Wnt/β-catenin 通路抑制 SOX6 表达，从而抑制 OGD/R 触发的 HT22 细胞损伤。而 SOX6 表达在 HIE 患者中上调。在 OGD/R 触发的 HT22 细胞中，MiR-19b-3p 过表达促进细胞增殖、抑制细胞凋亡、氧化应激反应和 Wnt/β-catenin 通路激活。MiR-19b-3p 负向调节 SOX6 表达。SOX6 敲低通过 Wnt/β-catenin 通路激活改善了 OGD/R 触发的 HT22 细胞损伤。MiR-19b-3p 过表达通过激活 Wnt/β-catenin 通路抑制 SOX6 表达，从而抑制 OGD/R 触发的 HT22 细胞损伤。SOX6 敲低通过 Wnt/β-catenin 通路激活改善了 OGD/R 触发的 HT22 细胞损伤。MiR-19b-3p 过表达通过激活 Wnt/β-catenin 通路抑制 SOX6 表达，从而抑制 OGD/R 触发的 HT22 细胞损伤。SOX6 敲低通过 Wnt/β-catenin 通路激活改善了 OGD/R 触发的 HT22 细胞损伤。MiR-19b-3p 过表达通过激活 Wnt/β-catenin 通路抑制 SOX6 表达，从而抑制 OGD/R 触发的 HT22 细胞损伤。