Hypoxic-ischemic encephalopathy (HIE) results in high neonatal mortality and severe neurological impairments, and its underlying molecular mechanism underwent extensive investigations. Long non-coding RNA (lncRNA) is considered to be an important regulator on brain development and many neurological diseases. Currently, little is known about the role of Vof-16 (lncRNA) in HIE. We detected the relative expression level of Vof-16 in the cortex and hippocampus of hypoxic-ischemic (HI) models whose successful establishment was verified by TTC staining. Then, Vof-16 knockout rats were generated using the CRISPR/Cas engineering technology to search the specific function of the Vof-16 through a series of behavioral evaluations including Neurological severity scores (NSS), Y-maze test, Morris water maze (MWW) test, open field test, and Rotarod test. The results demonstrated the expression of Vof-16 was substantially up-regulated in the cortex and hippocampus of rats with HI injury. Importantly, Vof-16 knockout facilitated the recovery from long-term HI induced nerve damage and neurobehavioral dysfunctions. In conclusion, this study suggests Vof-16 knockout is a promising treatment target for neonatal HIE.

缺氧缺血性脑病 (HIE) 导致高新生儿死亡率和严重的神经功能障碍，其潜在的分子机制经过广泛研究。长链非编码 RNA (lncRNA) 被认为是大脑发育和许多神经系统疾病的重要调节因子。目前，对 Vof-16 (lncRNA) 在 HIE 中的作用知之甚少。我们检测了缺氧缺血（HI）模型的皮层和海马中Vof-16的相对表达水平，其成功建立经TTC染色验证。然后，利用CRISPR/Cas工程技术生成Vof-16基因敲除大鼠，通过神经严重程度评分（NSS）、Y型迷宫试验、Morris水迷宫（MWW）等一系列行为评估，寻找Vof-16的具体功能) 试验、露天试验和 Rotarod 试验。结果表明，Vof-16 在 HI 损伤大鼠的皮层和海马中的表达显着上调。重要的是，Vof-16 敲除促进了长期 HI 诱导的神经损伤和神经行为功能障碍的恢复。总之，这项研究表明 Vof-16 敲除是新生儿 HIE 的一个有希望的治疗目标。