Spinosin protects Neuro-2a/APP695 cells from oxidative stress damage by inactivating p38.

Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan Pub Date : 2023-10-01 DOI:10.19852/j.cnki.jtcm.20220907.001

Zhang Xiaoying, Wang Ruixuan, Wang Yiqing, X U Fanxing, Yan Tingxu, W U Bo, Zhang Ming, Jia Ying

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Abstract

Objective: To explore the protective mechanism of spinosin (SPI) on Alzheimer's disease (AD) model cells, Neuro-2a/APP695 (N2a/APP695), against HO-induced oxidative stress damage, to reflect the influence of oxidative stress on the development of AD, and to provide a valuable basis for the research and development of therapeutic drug for AD.

Methods: N2a/APP695 cells were exposed to HO and then treated with spinosin. Firstly, the secretion level of amyloid β (Aβ) and the production of malondialdehyde (MDA) and lactate dehydrogenase (LDH) were detected by enzyme linked immunosorbent assay kits. Secondly, the oligomerization degree of Aβ was performed by Thioflavin T staining. Thirdly, the expression levels of p-Tau (Ser199/202/396), synaptophysin (SYP), postsynaptic density protein 95 (PSD95), and mitogen-activated protein kinase (MAPK) family-related proteins were detected by Western blot analysis. In addition, FITC-labeled phalloidin was used in cytoskeleton staining to reflect synaptic function.

Results: This study showed that HO stimulated N2a/APP695 cells to produce excessive MDA and LDH and secrete a large amount of Aβ, promoted the aggregation of Aβ, induced Tau protein hyperphosphorylation, and led to synaptic dysfunction. Spinosin reversed these changes caused by HO by inactivating p38, which was verified by treatment with the p38 inhibitor BIRB796.

Conclusion: Spinosin protects N2a/APP695 cells from oxidative stress damage caused by HO through inactivating p38.

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Spinosin通过失活p38保护Neuro-2a/APP695细胞免受氧化应激损伤。

目的：探讨刺突蛋白（SPI）对阿尔茨海默病（AD）模型细胞Neuro-2a/APP695（N2a/APP 695）对抗HO诱导的氧化应激损伤的保护机制，以反映氧化应激对AD发展的影响，为AD治疗药物的研究和开发提供有价值的依据。方法：将N2a/APP695细胞暴露于HO，然后用刺突蛋白处理。首先，用酶联免疫吸附试剂盒检测淀粉样蛋白β（Aβ）的分泌水平以及丙二醛（MDA）和乳酸脱氢酶（LDH）的产生。其次，用硫黄素T染色法测定Aβ的低聚程度。第三，通过蛋白质印迹分析检测p-Tau（Ser199/202/396）、突触素（SYP）、突触后密度蛋白95（PSD95）和丝裂原活化蛋白激酶（MAPK）家族相关蛋白的表达水平。此外，FITC标记的鬼笔肽用于细胞骨架染色以反映突触功能。结果：HO刺激N2a/APP695细胞产生过量的MDA和LDH，并分泌大量的aβ，促进aβ的聚集，诱导Tau蛋白过度磷酸化，导致突触功能障碍。Spinosin通过失活p38逆转了HO引起的这些变化，用p38抑制剂BIRB796处理证实了这一点。结论：Spinosin可通过失活p38保护N2a/APP695细胞免受HO引起的氧化应激损伤。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan

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