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首页> 外文期刊>BioMed research international >Protective Effects of p38 MAPK Inhibitor SB202190 against Hippocampal Apoptosis and Spatial Learning and Memory Deficits in a Rat Model of Vascular Dementia
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Protective Effects of p38 MAPK Inhibitor SB202190 against Hippocampal Apoptosis and Spatial Learning and Memory Deficits in a Rat Model of Vascular Dementia

机译：p38 MAPK抑制剂SB202190对血管性痴呆大鼠模型海马细胞凋亡和空间学习记忆障碍的保护作用

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Vascular dementia (VaD) is a common age-related neurodegenerative disease resulting from chronic hypoxia. In the present study, we examined the protective effects of p38 MAPK inhibitor SB202190 against hippocampal apoptosis and spatial learning and memory deficits in a chronic hypoperfusion rat model of VaD established by permanent bilateral carotid occlusion (2-VO). Sixty rats were randomly divided into sham-operated, VaD model, and VaD plus SB202190 groups (n=20/group). After sham/2-VO surgery, rats were administered 0.1% DMSO (sham-operated and VaD groups) or SB202190 by intracerebroventricular injection. One week after inhibitor/vehicle treatment, hippocampal p38 MAPK phosphorylation was higher in the model group than in the SB202190 group (P<0.01). Compared to the model group, the SB202190 group exhibited significantly shorter escape latencies in the Morris water maze hidden platform trials (P<0.01) and longer times in the original platform quadrant during probe trials (P<0.01). The SB202190 group also showed significantly reduced neuronal apoptosis in the hippocampus compared to VaD model rats (P<0.01) as well as higher (antiapoptotic) Bcl-2 expression and lower (proapoptotic) caspase-3 expression (P<0.01for both). In conclusion, blockade of the p38 MAPK signaling pathway by SB202190 following permanent 2-OV reduced apoptosis of hippocampal neurons and rescued spatial learning and memory deficits.
机译：血管性痴呆（VaD）是一种常见的与年龄相关的神经退行性疾病，由慢性低氧引起。在本研究中，我们研究了p38 MAPK抑制剂SB202190在永久性双侧颈动脉闭塞（2-VO）建立的VaD慢性低灌注大鼠模型中对海马凋亡和空间学习与记忆缺陷的保护作用。 60只大鼠随机分为假手术组，VaD模型组和VaD加SB202190组（n = 20 /组）。假/ 2-VO手术后，通过脑室内注射对大鼠施用0.1％DMSO（假手术组和VaD组）或SB202190。抑制剂/载体治疗一周后，模型组海马p38 MAPK磷酸化水平高于SB202190组（P <0.01）。与模型组相比，SB202190组在莫里斯水迷宫隐藏平台试验中表现出明显更短的逃逸潜伏期（P <0.01），而在探针试验期间在原始平台象限中表现出更长的逃逸潜伏期（P <0.01）。与VaD模型大鼠相比，SB202190组还显示出海马神经元凋亡显着减少（P <0.01），Bcl-2表达高（抗凋亡）和Caspase-3表达低（促凋亡）（两者均P <0.01）。总之，永久性2-OV后SB202190对p38 MAPK信号通路的阻断减少了海马神经元的凋亡，并挽救了空间学习和记忆障碍。

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