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AKT Phosphorylation - Europe PMC

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Last Updated: 13 June 2022

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Cryptotanshinone Attenuates Amyloid-β 42 -induced Tau Phosphorylation by Regulating PI3K/Akt/GSK3β Pathway in HT22 Cells.

"An Alzheimer's disease pathological features include the emergence of senile plaques as a result of amyloid-u03b2 deposition and neurofibrillary tangles caused by tau hyperphosphorylation. " For AD therapy, reducing tau hyperphosphorylation is vital. According to a network pharmacology review, CTS may reduce tau hyperphosphorylation by limiting the phosphatidylinositol 3 kinases/protein kinase B/ glycogen synthase pathway through the nase-3 pathway. The expression of tau and related proteins in the PI3K/Akt/GSK3b2 pathway were determined by using western blot and immunofluorescence staining. CTS has significantly reduced tau hyperphosphorylation in Ser202, Ser404, Thr181, and Thr231 cell models in A&O- and OKA-induced cell cultures, according to our results. CTS had neuroprotective advantages by banning the PI3K/Akt/GSK3 signaling pathway, according to the study, which showed that CTS exerted neuroprotective activity by limiting the PI3K/Akt/GSK3+ signaling pathway. In HT22 cells, we reported for the first time that CTS inhibited AD-related tau hyperphosphorylation and reduced the effects of Au03b2O on the expression of PSD95 and synaptophysin by the PI3K/Akt/GSK3b2 pathway.

Source link: https://europepmc.org/article/MED/35575872

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions