Our study aimed to explore the function and mechanism of action of long noncoding RNA (lncRNA) SRY-Box 21 antisense RNA 1 (SOX21-AS1) in amyloid beta_25–35 (Aβ_25–35)-induced neuronal damage. To induce neuronal damage, neuronal cells and differentiated IMR-32 neuroblastoma cells were challenged by Aβ_25–35. SOX21-AS1 and miR-132 quantities were detected by quantitative reverse transcription polymerase chain reaction. Cell damage was evaluated by detecting the changes of cell viability, apoptosis, and oxidative stress. Cell viability was measured using cell counting kit-8. Cell apoptosis was evaluated by flow cytometry and caspase-3 activity. The oxidative stress was analyzed by reactive oxygen species level. The expression of proteins associated with the phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) pathway was examined by western blot. SOX21-AS1 abundance was up-regulated in Aβ_25–35-challenged neuronal cells. Silencing of SOX21-AS1 attenuated Aβ_25–35-induced viability reduction and promotion of apoptosis and oxidative stress, suggesting that silencing of SOX21-AS1 repressed Aβ_25–35-induced neuronal damage. miR-132 quantity was reduced in Aβ_25–35-challenged neuronal cells, and negatively controlled by SOX21-AS1. miR-132 knockdown abolished the effect of SOX21-AS1 silencing on Aβ_25–35-induced neuronal damage, indicating that SOX21-AS1 controls Aβ_25–35-induced neuronal damage via regulating miR-132. The PI3K/AKT signaling was repressed in Aβ_25–35-challenged cells, but this effect was counteracted upon overexpression of miR-132. In conclusion, SOX21-AS1 knockdown mitigated Aβ_25–35-dependent neuronal cell damage by promoting miR-132/PI3K/AKT pathway.

我们的研究旨在探索长链非编码 RNA (lncRNA) SRY-Box 21 反义 RNA 1 (SOX21-AS1) 在 β _25-35 (Aβ _25-35 ) 诱导的神经元损伤中的功能和作用机制。为了诱导神经元损伤，神经元细胞和分化的 IMR-32 神经母细胞瘤细胞受到 Aβ _{25-35 的}挑战. 通过定量逆转录聚合酶链反应检测 SOX21-AS1 和 miR-132 的数量。通过检测细胞活力、细胞凋亡和氧化应激的变化来评估细胞损伤。使用细胞计数试剂盒-8 测量细胞活力。通过流式细胞术和 caspase-3 活性评估细胞凋亡。通过活性氧水平分析氧化应激。通过蛋白质印迹检查与磷酸肌醇 3-激酶 (PI3K)/蛋白激酶 B (AKT) 途径相关的蛋白质的表达。SOX21-AS1 丰度在 Aβ _25-35攻击的神经元细胞中上调。SOX21-AS1 的沉默减弱了 Aβ _25-35诱导的活力降低和细胞凋亡和氧化应激的促进，表明 SOX21-AS1 的沉默抑制了 Aβ _25-35诱导的神经元损伤。Aβ _25-35攻击的神经元细胞中miR-132 的数量减少，并受 SOX21-AS1 的负控制。miR-132 敲低消除了 SOX21-AS1 沉默对 Aβ _25-35诱导的神经元损伤的影响，表明 SOX21-AS1通过调节 miR-132 来控制 Aβ _25-35诱导的神经元损伤。PI3K/AKT 信号在 Aβ _25-35攻击的细胞中受到抑制，但这种影响在 miR-132 的过表达时被抵消。总之，SOX21-AS1 敲低减轻了 Aβ _25-35通过促进 miR-132/PI3K/AKT 通路来抑制依赖的神经元细胞损伤。