青蒿琥酯与美金刚在氯化铝诱导大鼠神经毒性模型中的作用

A. Shata, W. Elkashef, M. Hamouda, H. Eissa
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引用次数: 4

摘要

阿尔茨海默病是最常见的神经系统疾病之一,其特征是淀粉样斑块在多脑区积聚。本研究探讨了青蒿琥酯对铝致大鼠神经毒性与美金刚的潜在神经保护作用。将40只雄性白化Wistar大鼠随机分为4组:1组为阴性对照组,2组为氯化铵诱导的阳性对照组,3组为NH4Cl +青蒿琥酯溶液处理,4组为NH4Cl +美金刚sc处理,采用Morris水迷宫(MWM)试验评价空间记忆和学习能力。测定大脑皮层组织匀浆中丙二醛(MDA)和还原型谷胱甘肽(GSH)水平。采用大鼠酶联免疫吸附试验(ELISA)试剂盒测定大鼠大脑皮层组织匀浆中肿瘤坏死因子-α (TNFα)和白细胞介素-1β (IL-1β)的浓度。实时定量逆转录聚合酶链反应(Real-time qRT-PCR)检测大鼠大脑皮层Caspase-3、Bcl-2和iNOS基因的表达。对大鼠大脑皮层切片进行组织病理学检查。青蒿琥酯显著降低大脑皮层MDA水平,抑制iNOS、caspase,上调Bcl-2基因表达。ART显著提高抗氧化GSH水平,显著降低tnf - α和IL-B水平。它显著降低了1ry留存延迟、2ry留存延迟和初始获取延迟。它还能改善脑组织病理学,减少淀粉样斑块沉积。ART通过调节氧化应激和增强大脑皮层神经元细胞的抗凋亡标志物发挥神经保护作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Effect of Artesunate vs Memantine in Aluminum Chloride Induced Model of Neurotoxicity in Rats
Alzheimer disease is one of the commonest neurological diseases which is characterized by amyloid plaques accumulation in multiple brain regions. This study investigated the potential neuroprotective effect of artesunate on aluminum induced neurotoxicity vs memantine in rats. 40 male albino Wistar rats were divided randomly into 4 groups as follow: Group 1 negative control, group 2 positive control group induced by ammonium chloride, group 3 rats treated by NH4Cl + artesunate solution, group 4 rats treated by NH4Cl + memantine S.C. spatial Memory and Learning were evaluated using Morris Water Maze (MWM) test. Malondialdehyde (MDA) and reduced glutathione (GSH) levels were measured in cerebral cortex tissue homogenate. Tumor necrosis factor-α (TNFα) and interleukin-1 beta (IL-1β) concentrations were measured in rat cerebral cortex tissue homogenate using rat enzyme linked immunosorbent assay (ELISA) kits. Real-time quantitative reverse transcription-polymerase chain reaction (Real-time qRT-PCR) for Caspase-3, Bcl-2 and iNOS gene expression was measured in rat cerebral cortex. Slices from cerebral cortex were studied by histopathological examination. Artesunate significantly decreased MDA level and inhibited iNOS, caspase and upregulated Bcl-2 gene expression in cerebral cortex. ART increased significantly antioxidant level GSH, and decreased significantly TNF-alpha and IL-B levels. It reduced significantly 1ry retention latency, 2ry retention latency and initial acquisition latency. It also improved brain histopathology and decreased amyloid plaque deposition. ART exerted neuroprotective effect through oxidative stress correction and enhancement of antiapoptotic markers in neuronal cells of the cerebral cortex.
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