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首页> 外文期刊>Drug Design, Development and Therapy >Nimodipine Improves Cognitive Impairment After Subarachnoid Hemorrhage in Rats Through IncRNA NEAT1/miR-27a/MAPT Axis
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Nimodipine Improves Cognitive Impairment After Subarachnoid Hemorrhage in Rats Through IncRNA NEAT1/miR-27a/MAPT Axis

机译：通过IncRNA Neat1 / miR-27a / maMT轴在大鼠蛛网膜下腔出血后提高了尼莫氏脂提高了认知障碍

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Background: Subarachnoid hemorrhage (SAH) is a cerebral hemorrhage disease that severely damages the brain and causes cognitive impairment (CI). Therefore, accurate and appropriate treatment strategies are urgently needed. The application of nimodipine can not only improve blood circulation in patients with SAH but also repair ischemic neuron injury. Purpose: To investigate the effects of nimodipine and lncRNA nuclear paraspeckle assembly transcript 1 (NEAT1)/miR-27a/microtubule-associated protein tau (MAPT) axis on CI after SAH. Methods: One hundred and twenty healthy male rats were selected and equally divided into control group, sham operation group, model group, PBS group, nimodipine group (drug group), NC siRNA group, NC mimics group, NEAT1 siRNA, miR-27a mimics, MAPT siRNA, drug + NEAT1-ad, and drug + NC-ad groups by random number table. Rats in the model group were constructed by double-hemorrhage model, and expression vectors were injected into the tail to regulate the expression of lncRNA NEAT1, miR-27a and MAPT. In addition, Western blot was employed to detect brain tissue protein, flow cytometry was applied to measure brain tissue apoptosis, and MTT was utilized to determine cell activity, so as to evaluate brain damage and cognitive function in each group. Results: Nimodipine, down-regulated lncRNA NEAT1, up-regulated miR-27a and down-regulated MAPT all improved brain damage and CI, inhibited brain tissue cell apoptosis, and enhanced brain cell activity. The common binding sites of lncRNA NEAT1 and MAPT were found on the miR-27a sequence fragment, and miR-27a could be paired with the former two. Nimodipine was found to cause the down-regulation of lncRNA NEAT1 and MAPT, as well as the up-regulation of miR-27a. Conclusion: Nimodipine can improve CI after SAH in rats through the lncRNA NEAT1/miR-27a/MAPT axis.
机译：背景：蛛网膜下腔出血（SAH）是一种严重损害大脑的脑出血疾病，并导致认知障碍（CI）。因此，迫切需要准确和适当的治疗策略。尼莫氏脂的应用不仅可以改善SAH患者的血液循环，还可以修复缺血神经元损伤。目的：探讨尼莫地平和LNCRNA核心腺素包装组件转录物1（NEAT1）/ miR-27A /微管相关蛋白TAU（MAPT）轴在CI之后的效果。方法：选择一百二十个健康的雄性大鼠，同等为对照组，假手术组，模型组，PBS组，奈代疟原（药物组），NC siRNA组，NC模拟组，Neat1 siRNA，MiR-27A模拟，Mapt siRNA，药物+ Neat1-AD和药物+ NC-AD组通过随机数表。模型组中的大鼠通过双出血模型构建，并将表达载体注射到尾部以调节LNCRNA Neat1，miR-27a和Mapt的表达。此外，使用蛋白质印迹来检测脑组织蛋白质，施用流式细胞术以测量脑组织凋亡，并且使用MTT来确定细胞活性，以评估每组的脑损伤和认知功能。结果：Nimodipine，下调的LNCRNA Neat1，上调的MiR-27a和下调Mapt所有改善的脑损伤和CI，抑制脑组织细胞凋亡，增强脑细胞活性。在miR-27a序列片段上发现LNCRNA Neat1和MapT的常用粘合位点，并且MiR-27a可以与前两者配对。发现Nimodipine导致LNCRNA Neat1和MAPT的下调，以及miR-27a的上调。结论：通过LNCRNA Neat1 / miR-27a / MaMT轴线在大鼠中的SAH后可以改善CI的CI。

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