| 朱 婧,李 鑫,朱利娟,康 涛,高 娜.右美托咪啶通过抑制线粒体功能障碍衍生的氧化应激保护宫内窘迫新生鼠的脑功能障碍的机制[J].,2021,(18):3426-3430 |
| 右美托咪啶通过抑制线粒体功能障碍衍生的氧化应激保护宫内窘迫新生鼠的脑功能障碍的机制 |
| The Mechanism of Dexmedetomidine Protects the Brain Dysfunction of Neonatal Rats with Intrauterine Distress by Inhibiting Oxidative Stress Derived from Mitochondrial Dysfunction |
| 投稿时间：2021-02-26 修订日期：2021-03-22 |
| DOI：10.13241/j.cnki.pmb.2021.18.006 |
| 中文关键词: 宫内窘迫 线粒体 氧化应激 脑损伤 右美托咪啶 |
| 英文关键词: Intrauterine distress Mitochondria Oxidative stress Brain damage Dexmedetomidine |
| 基金项目:陕西省自然科学基础研究计划项目（2018JM7121） |
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| 中文摘要: |
| 摘要 目的：探讨右美托咪啶通过抑制线粒体功能障碍衍生的氧化应激保护宫内窘迫新生鼠的脑功能障碍的机制。方法：24周龄Sprague-Dawley大鼠，按照雌雄比= 1：2的饲养于笼中自然受孕，对确定受孕的大鼠进行宫内窘迫模型手术，然后分为对照组、宫内窘迫组和右美托咪啶组。通过莫里斯水迷宫测试测和牵引力测试分别检测大鼠的学习能力、运动能力。使用电子分析天平检测大鼠脑含水量，通过FJB染色确定退化神经元的数目。通过商购试剂盒检测大鼠氧化应激指标谷胱甘肽过氧化物酶（Glutathione peroxidase, GPx）、丙二醛（Malondialdehyde, MDA）和还原型辅酶Ⅱ（Nicotinamide adenine dinucleotide, NADPH）的含量。通过蛋白印迹分析Hsp90和p-AKT Thr 308的蛋白表达。通过RT-PCR分析线粒体介导的神经元凋亡相关因子caspase-3、Bax和Bcl-2的mRNA表达。结果：与对照组相比，宫内窘迫组迷宫测试用时、脑水含量、退化神经元量、MDA和NADPH含量以及caspase-3和Bax的mRNA表达均显著增加，牵引力得分、Hsp90和p-AKT Thr 308的蛋白表达以及Bcl-2mRNA表达均显著降低（P<0.05），而与宫内窘迫组相比，右美托咪啶组迷宫测试用时、脑水含量、退化神经元量、MDA和NADPH含量以及caspase-3和Bax的mRNA表达均显著减少，牵引力得分、Hsp90和p-AKT Thr 308的蛋白表达以及Bcl-2mRNA表达均显著增加（P<0.05）。结论：右美托咪啶减轻了宫内窘迫大鼠的线粒体功能障碍，进而抑制了氧化应激并改善了大鼠的神经功能缺损和脑损伤。 |
| 英文摘要: |
| ABSTRACT Objective: To investigate the mechanism of dexmedetomidine to protect the brain dysfunction of neonatal rats with intrauterine distress by inhibiting oxidative stress derived from mitochondrial dysfunction. Methods: Sprague-Dawley rats at the age of 24 weeks were conceived naturally in cages with a ratio of female to male = 1:2. Intrauterine distress model surgery was performed on the rats with confirmed conception, and then they were divided into control group, intrauterine distress group and dexmedetomidine group. Morris water maze test and traction test were used to detect the learning ability and exercise ability of rats. An electronic analytical balance was used to detect the water content of the rat brain, and the number of degenerative neurons was determined by FJB staining. The levels of oxidative stress indicators glutathione peroxidase (GPx), malondialdehyde (MDA) and nicotinamide adenine dinucleotide phosphate(NADPH) were detected by commercially available kits. The protein expression of Hsp90 and p-AKT Thr 308 was analyzed by Western blot. The mRNA expression of caspase-3, Bax and Bcl-2 related to mitochondria-mediated neuronal apoptosis was analyzed by RT-PCR. Results: Compared with the control group, the maze test time, brain water content, degenerative neuron content, MDA and NADPH content, and the mRNA expression of caspase-3 and Bax in the intrauterine distress group were significantly increased, while the traction score, protein expression of Hsp90 and p-AKT Thr 308, and Bcl-2mRNA expression were all significantly reduced (P<0.05); Compared with the intrauterine distress group, the dexmedetomidine group had a significant decrease in maze test time, brain water content, degenerative neuron content, MDA and NADPH content, and caspase-3 and Bax mRNA expression, while the traction score, protein expression of Hsp90 and p-AKT Thr 308, and Bcl-2 mRNA expression all increased significantly (P<0.05). Conclusion: Dexmedetomidine reduces mitochondrial dysfunction in rats with intrauterine distress, thereby inhibiting oxidative stress and improving neurological deficits and brain damage in rats. |
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