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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| http://dx.doi.org/10.19852/j.cnki.jtcm.20220907.001 | DOI Listing |
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