Wang L、Fu G、Han R、Fan P、Yang J、Gong K、Zhao Z、Zhang C、Sun K、Shao GMALAT1 和 NEAT1 在小鼠海马缺氧预适应期间可能通过 NR2B High Alt Med Biol 的调节发挥神经保护作用。 00:000-000, 2024。背景：非编码核糖核酸 (ncRNA) 的调节已被证明参与对缺氧预适应 (HPC) 的细胞和分子反应，这是一种由大脑中诱导亚致死缺氧引起的情况。 ncRNA 转移相关肺腺癌转录本 1 (MALAT1) 和核旁斑组装转录本 1 (NEAT1) 在大脑中大量表达，它们调节神经细胞中各种基因的表达。然而，MALAT1 和 NEAT1 在 HPC 中的确切作用尚不完全清楚。方法：采用急性反复缺氧小鼠模型作为HPC模型，采用实时聚合酶链式反应（PCR）测定海马MALAT1和NEAT1水平。分别使用实时 PCR 和蛋白质印迹法测量小鼠海马中 N-甲基-d-天冬氨酸受体亚基 2 B (NR2B) 的 mRNA 和蛋白质水平。敲低 MALAT1 和 NEAT1 的 HT22 细胞用于体外测试。还评估了参与缺血和缺氧条件下神经细胞损伤的 NR2B 的表达。通过蛋白质印迹法测定氧糖剥夺/再灌注 (OGD/R) 下 MALAT1 和 NEAT1 敲低 HT22 细胞中血影蛋白和裂解的 caspase-3 的水平。结果：HPC 增加了小鼠海马中 MALAT1 和 NEAT1 的表达，并降低了 NR2B mRNA 的表达（p < 0.05）。 MALAT1 和 NEAT1 的敲低使 NR2B mRNA 和蛋白质水平增加近两倍，并在 OGD/R 条件下对 HT22 细胞造成损伤 (p < 0.05)。结论：MALAT1和NEAT1通过影响NR2B的表达发挥神经保护作用。

Wang L, Fu G, Han R, Fan P, Yang J, Gong K, Zhao Z, Zhang C, Sun K, Shao GMALAT1 and NEAT1 Are Neuroprotective during Hypoxic Preconditioning in the Mouse Hippocampus Possibly by Regulation of NR2B High Alt Med Biol. 00:000-000, 2024. Background: The regulation of noncoding ribonucleic acid (ncRNA) has been shown to be involved in cellular and molecular responses to hypoxic preconditioning (HPC), a situation created by the induction of sublethal hypoxia in the brain. The ncRNAs metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) and nuclear paraspeckle assembly transcript 1 (NEAT1) are abundantly expressed in the brain, where they regulate the expression of various genes in nerve cells. However, the exact roles of MALAT1 and NEAT1 in HPC are not fully understood. Methods: A mouse model of acute repeated hypoxia was used as a model of HPC, and MALAT1 and NEAT1 levels in the hippocampus were measured using real-time polymerase chain reaction (PCR). The mRNA and protein levels of N-methyl-d-aspartate receptor subunit 2 B (NR2B) in the mouse hippocampus were measured using real-time PCR and western blotting, respectively. HT22 cells knocked-down for MALAT1 and NEAT1 were used for in vitro testing. Expression of NR2B, which is involved in nerve cell injury under ischemic and hypoxic conditions, was also evaluated. The levels of spectrin and cleaved caspase-3 in MALAT1 and NEAT1 knockdown HT22 cells under oxygen glucose deprivation/reperfusion (OGD/R) were determined by western blotting. Results: HPC increased the expression of MALAT1 and NEAT1 and decreased the expression of NR2B mRNA in the mouse hippocampus (p < 0.05). Knockdown of MALAT1 and NEAT1 increased both NR2B mRNA and protein levels nearly twofold and caused damage under OGD/R conditions in HT22 cells (p < 0.05). Conclusion: MALAT1 and NEAT1 exert neuroprotective effects by influencing the expression of NR2B.