| 陈辉,赵春水,张春伟,等.微 RNA-24过表达对缺血性脑梗死大鼠的脑保护作用及对神经细胞凋亡的影响[J].安徽医药,2023,27(9):1787-1791. |
| 微 RNA-24过表达对缺血性脑梗死大鼠的脑保护作用及对神经细胞凋亡的影响 |
| Cerebroprotective effect of microRNA-24 overexpression on ischemic cerebral infarction in rats and its effect on neuronal cell apoptosis |
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| DOI：10.3969/j.issn.1009-6469.2023.09.020 |
| 中文关键词: 脑梗死 脑缺血 脑保护作用 神经细胞凋亡 微 RNA-24 |
| 英文关键词: Brain infarction Brain ischemia Cerebroprotective effect Neuronal apoptosis MicroRNA-24 |
| 基金项目:河南省医学科技攻关计划项目( 201504078) |
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| 中文摘要: |
| 目的研究微 RNA(miR)-24过表达对缺血性脑梗死( ICI)大鼠的脑保护作用及对神经细胞凋亡的影响，并探讨相关机制。方法 2020年 1月至 2022年 1月将 45只大鼠以随机数字表法分为健康组(注射生理盐水)、脑梗死组(注射生理盐水)、梗死过表达组(注射 miR-24 agomir)、脑梗死低表达组(注射 miR-24 antagomir)、脑梗死阴性对照( NC)组(注射 miR-24-NC)。注脑射后 24 h建立 ICI模型，最终各组均纳入 8只。建模成功后 1、3d评价大鼠神经功能；实时荧光定量逆转录聚合酶链反应( qRTPCR)检测脑组织 miR-24 mRNA表达； TTC染色法检测脑梗死体积；免疫组织化学染色法检测脑皮质神经元核抗原( NeuN)表达；蛋白质印迹法检测脑组织 B细胞淋巴瘤 -2(Bcl-2)、 Bcl-2相关 X蛋白( Bax)蛋白表达。结果与脑梗死组( 2.06±0.25)分、(1.72±0.19)分比较，建模后 1、3d脑梗死过表达组 Zea-longa神经功能评分( 0.98±0.11)分、(0.82±0.09)分降低，脑梗死低表达组(2.71±0.24)分、(2.36±0.21)分升高( P<0.05)。与健康组 0.56±0.12比较，脑梗死组脑组织 miR-24 mRNA表达 0.21±0.03降低(P<0.05)；与脑梗死组比较，脑梗死过表达组脑组织 miR-24 mRNA表达 1.38±0.26升高( P<0.05)脑梗死低表达组 0.06±0.01降低(P<0.05)。与脑梗死组( 40.31±5.30)mm3(292.20±35.60)个 /视野、 0.13±0.02、0.52±0.06比脑梗死过表达组脑梗死体积较(21.25±4.93)mm3缩小，脑梗死皮质区 NeuN性表达神经元数目( 385.20±45.13)个 /视野增加，脑组织 Bcl-2蛋白表达 0.54±0.07升高， Bax蛋白表达 0.36±0.04降低，脑梗死低表达组脑梗死体积( 50.56±6.14)mm3增大，脑梗死皮质区 NeuN阳性表达神经元数目(154.40±17.91)个 /视野减少， Bcl-2蛋白表达 0.05±0.01降低， Bax蛋白表达 0.69±0.07升高( P<0.05)。结论 miR-24过表达可阳、改善 ICI大鼠神经功能，缩小脑梗死体积，减少神经元凋亡，可能通过调节脑组织 Bcl-2、Bax蛋白表达来实现。 |
| 英文摘要: |
| Objective To investigate the cerebroprotective effect of microRNA (miR)-24 overexpression on ischemic cerebral infarc-tion (ICI) rats and the influence on neuronal apoptosis and to explore the related mechanisms.Methods From January 2020 to January2022, 45 rats were randomly divided into a healthy group (injection with saline), a cerebral infarction group (injection with saline), a ce-rebral infarction overexpression group (injection with miR-24 agomir), a cerebral infarction low-expression group (injection with miR24 antagomir), and a cerebral infarction negative control (NC) group (injection with negative sequence) using a random number tablemethod. The ICI model was established 24 h after injection, and finally 8 rats were included in each group. The neurological function ofthe rats was evaluated 1 and 3 d after successful modeling. Real-time fluorescence quantitative reverse transcription polymerase chain reaction (qRT-PCR) was used to detect miR-24 mRNA expression in brain tissue; TTC staining was used to detect cerebral infarctionvolume; immunohistochemical staining was used to detect neuronal nuclear antigen (NeuN) expression in the cerebral cortex; and pro-tein blotting was used to detect B-cell lymphoma-2 (Bcl-2), and Bcl-2-related X protein (Bax) protein expression in brain tissue.Re- sults Compared with the cerebral infarction group (2.06±0.25 and 1.72±0.19), the Zea-Longa neurological function scores were lowerin the cerebral infarction overexpression group (0.98±0.11 and 0.82±0.09) at 1 and 3 d after modeling and higher in the cerebral infarc-tion overexpression group (2.71±0.24 and 2.36±0.21) (P<0.05). Compared with the healthy group (0.56±0.12), brain tissue miR-24 mRNA expression in the cerebral infarction group (0.21±0.03) was decreased (P<0.05); compared with the cerebral infarction group, brain tissue miR-24 mRNA expression in the cerebral infarction overexpression group (1.38±0.26) was elevated (P<0.05), and that in the cerebral infarction low-expression group (0.06±0.01) decreased (P<0.05). Compared with the cerebral infarction group (40.31±5.30) mm3, (292.20±35.60) neurons/field of view, 0.13±0.02, 0.52±0.06, cerebral infarction volume in the cerebral infarction overexpression group (21.25±4.93) mm3 was reduced, the number of neurons positively expressed in the cortical area of cerebral infarction (385.20±45.13) neurons/field of view increased, brain tissue Bcl-2 protein expression (0.54±0.07) increased, Bax protein expression (0.36±0.04)decreased, and cerebral infarction volume (50.56±6.14) mm3 increased in the cerebral infarction low-expression group, and the number of NeuN-positively expressing neurons in the cerebral infarction cortical area (154.40±17.91) decreased/field of view, and Bcl-2 protein expression (0.05±0.01) decreased and Bax protein expression (0.69±0.07) increased (P<0.05).Conclusion The overexpression of miR24 can improve neurological function, reduce the volume of cerebral infarction and decrease neuronal apoptosis in ICI rats, possibly byregulating the expression of Bcl-2 and Bax proteins in brain tissue. |
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