β-asarone Protects p-tau from Okadaic Acid in PC12 Cells by Activating PP2A and Involving Akt/mTOR/Beclin-1 Pathway

作者：Huang, Liping; Zhong, Xiaoqin; Xu, Yuanhang; Deng, Minzhen^*; Zhou, Zhongliu^*

来源：Pharmacognosy Magazine, 2023, 19(3): 727-735.

DOI：10.1177/09731296231168743

• beta-asarone
• tau hyperphosphorylation
• okadaic acid
• PC12 cell
• Alzheimer's disease

Background The aggregation of tau hyperphosphorylation (p-tau) into neurofibrillary tangles (NFT) is a hallmark in the histopathology of Alzheimer's disease (AD). Our previous experiments found that beta-asarone could prevent injury of PC12 cells induced by A (1-42), but could it fight cell damage of p-tau induced by okadaic acid (OA) is poorly understood. @@@ Objectives The emphasis of this study lies in beta-asarone's therapeutical effect on p-tau inhibition stimulated by OA. @@@ Materials and Methods 175 nmol OA was used to establish AD cells. Cell viability rate and cell toxicity were evaluated by the CCK-8 kit and LDH kit, respectively. The p-tau, A beta(42), beta-secretase, and protein phosphatase 2A (PP2A) were examined by ELISA. Proteins closely related to the pathogenesis of AD are involved p-tau, Beclin-1, p-Akt, and p-mTOR were analyzed by western-blotting and immunofluorescence detection. @@@ Results The results revealed that beta-asarone enhanced cell viability induced by OA in a dose-dependent manner. Moreover, compared to the OA model, p-tau, A beta(42), beta-secretase, and Beclin-1 were reduced, while PP2A, p-Akt, and p-mTOR increased after treatment with beta-asarone. @@@ Conclusion All data suggested that beta-asarone decreased p-tau, A beta(42), and beta-secretase levels, and activated PP2A levels by inhibiting Beclin-1-dependent autophagy in OA model cells, involving Akt/mTOR/Beclin-1 pathway.

• 单位
  广东省人民医院; 1; 广州中医药大学