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Cryptotanshinone Attenuates Amyloid-β42-induced Tau Phosphorylation by Regulating PI3K/Akt/GSK3β Pathway in HT22 Cells.

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机构： [1]Innovation Center for Neurological Disorders and Department of Neurology, Xuanwu Hospital, National Clinical Research Center for Geriatric Diseases, Capital Medical University, 45 Changchun Street, Beijing, China [2]Beijing Key Laboratory of Geriatric Cognitive Disorders, Beijing, China [3]Clinical Center for Neurodegenerative Disease and Memory Impairment, Capital Medical University, Beijing, China [4]Center of Alzheimer’s Disease, Beijing Institute of Brain Disorders, Collaborative Innovation Center for Brain Disorders, Capital Medical University, Beijing, China [5]Key Laboratory of Neurodegenerative Diseases, Ministry of Education, Beijing, China

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The pathological characteristics of Alzheimer's disease (AD) include formation of senile plaques resulting from amyloid-β (Aβ) deposition and neurofibrillary tangles caused by tau hyperphosphorylation. Reducing tau hyperphosphorylation is crucial for treatment of AD. Network pharmacology analysis showed that CTS may reduce tau hyperphosphorylation by regulating the phosphatidylinositol 3 kinases/protein kinase B/ glycogen synthase kinase-3β (PI3K/Akt/GSK3β) pathway. We investigated the ability of cryptotanshinone (CTS) to reduce Aβ-induced tau hyperphosphorylation and characterized the underlying mechanisms. Amyloid-β42 oligomers (AβO) were used to establish an AD model in HT22 cells. The expression levels of tau and related proteins in PI3K/Akt/GSK3β pathway were measured using western blot and immunofluorescence staining. The above-mentioned proteins were then evaluated in an okadaic acid (OKA)-induced AD cell model to verify the results. Synapse-associated proteins including post-synaptic density protein-95 (PSD95) and synaptophysin were also evaluated. We found that CTS significantly reduced tau hyperphosphorylation at Ser202, Ser404, Thr181, and Thr231 in AβO- and OKA-induced cell models. Moreover, we also found that CTS reversed AβO-induced reductions in the levels of PSD95 and synaptophysin. We used LY294002 to block PI3K and the results showed that CTS exerted neuroprotective effects through regulation of the PI3K/Akt/GSK3β signaling pathway. In summary, we showed for the first time that CTS inhibited AD-related tau hyperphosphorylation and reduced the effects of AβO on the expression levels of PSD95 and synaptophysin via the PI3K/Akt/GSK3β pathway in HT22 cells.© 2022. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.

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出版当年[2021]版：

大类 | 2 区医学

小类 | 2 区神经科学

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大类 | 2 区医学

小类 | 2 区神经科学

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Q1 NEUROSCIENCES

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Q1 NEUROSCIENCES

影响因子： 4.6 最新[2023版] 4.7 最新五年平均 5.59 出版当年[2020版] 5.512 出版当年五年平均 4.5 出版前一年[2019版] 5.686 出版后一年[2021版]

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第一作者机构： [1]Innovation Center for Neurological Disorders and Department of Neurology, Xuanwu Hospital, National Clinical Research Center for Geriatric Diseases, Capital Medical University, 45 Changchun Street, Beijing, China

通讯作者：

通讯机构： [1]Innovation Center for Neurological Disorders and Department of Neurology, Xuanwu Hospital, National Clinical Research Center for Geriatric Diseases, Capital Medical University, 45 Changchun Street, Beijing, China [2]Beijing Key Laboratory of Geriatric Cognitive Disorders, Beijing, China [3]Clinical Center for Neurodegenerative Disease and Memory Impairment, Capital Medical University, Beijing, China [4]Center of Alzheimer’s Disease, Beijing Institute of Brain Disorders, Collaborative Innovation Center for Brain Disorders, Capital Medical University, Beijing, China [5]Key Laboratory of Neurodegenerative Diseases, Ministry of Education, Beijing, China

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