Department of Anesthesiology, Beijing Hospital of Traditional Chinese Medicine, Capital Medical University, Beijing 100010, China.
Department of Anesthesiology, Beijing Hospital of Traditional Chinese Medicine, Capital Medical University, Beijing 100010, China.
Life Sci. 2021 Apr 15;271:119111. doi: 10.1016/j.lfs.2021.119111. Epub 2021 Jan 26.
Sevoflurane (Sevo) is neuroprotective in brain damage, thus our objective was to further investigate the impact of Sevo treatment on nerve regeneration and repair of neurological deficit in brain damage rats by regulating miR-490-5p and cyclin-dependent kinases 1 (CDK1).
The rat middle cerebral artery occlusion model was established. miR-490-5p and CDK1 levels in brain tissues were tested. The behavioral changes, the number of glial fibrillary acidic protein (GFAP) positive cells, ionized calcium-binding adapter molecule-1 (Iba-1) and Nestin mRNA expression, the survival and apoptosis of neurons in peripheral tissues of infarct areas were detected by a series of assays. Furthermore, the target relationship between miR-490-5p and CDK1 was verified.
miR-490-5p was reduced and CDK1 was raised in brain tissues of brain damage rats. Sevo raised miR-490-5p and decreased CDK1 to improve neurological deficits, reduce apoptotic neurons, suppress expression levels of GFAP and Iba-1, and increase Nestin expression and the number of surviving neurons in peripheral tissue in infarct area, and alleviate the pathological changes of brain tissues of brain damage rats. CDK1 was negatively regulated by miR-490-5p.
Our study presents that Sevo treatment is involved in neurogenesis and repair of neurological deficit of brain damage rats via up-regulating miR-490-5p and inhibiting CDK1.
七氟醚（Sevo）在脑损伤中具有神经保护作用，因此我们的目的是通过调节 miR-490-5p 和细胞周期蛋白依赖性激酶 1（CDK1），进一步研究 Sevo 治疗对脑损伤大鼠神经再生和神经功能缺损修复的影响。
建立大鼠大脑中动脉闭塞模型。检测脑组织中 miR-490-5p 和 CDK1 水平。通过一系列检测，检测行为变化、胶质纤维酸性蛋白（GFAP）阳性细胞数量、离子钙结合衔接分子-1（Iba-1）和巢蛋白 mRNA 表达、梗死区周围组织神经元的存活和凋亡。此外，验证了 miR-490-5p 和 CDK1 之间的靶向关系。
脑损伤大鼠脑组织中 miR-490-5p 减少，CDK1 升高。Sevo 升高 miR-490-5p 并降低 CDK1，以改善神经功能缺损，减少凋亡神经元，抑制 GFAP 和 Iba-1 的表达水平，增加梗死区周围组织中巢蛋白的表达和存活神经元的数量，并减轻脑损伤大鼠脑组织的病理变化。CDK1 受 miR-490-5p 负调控。
我们的研究表明，Sevo 治疗通过上调 miR-490-5p 和抑制 CDK1 参与脑损伤大鼠的神经发生和神经功能缺损修复。
