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.
基金：
Lingnan Normal University-level
talent project (grant no. ZL1801); The Natural Science Foundation
of Guangdong province of China (grant no. 2018A030307037); The
National Natural Science Foundation of China (grant nos. 31670363,
81904104 and 31900297); The Science and Technology Planning
Project of Guangdong Province, China (grant no. 2014A020221057);
The key discipline research project of Guangdong Province (2019
GDXK-0025 and 2021ZDJS035); The Yanling excellent young
teacher program of Lingnan Normal University (YL20200210) and
National Training Program of Innovation and Entrepreneurship for
Undergraduates (202010579006); The foundation of Education
Bureau of Guangdong Province (2015KTSCX087); The Postdoctoral
Foundation of China, (2021M690759) and The Administration of
Traditional Chinese Medicine of Guangdong Province, China
(20211203), the Open Project of Mangrove Institute, Lingnan
Normal University (grant no. YBXM01); the Open Project of
Western Guangdong Characteristic Biology and Medicine
Engineering and Research Center (grant no. 2022K03).
第一作者机构：[1]Lingnan Normal Univ, Western Guangdong Characterist Biomed Engn Technol, Sch Chem & Chem Engn, Zhanjiang, Peoples R China[2]Lingnan Normal Univ, Mangrove Inst, Dept Pharmaceut Engn, Zhanjiang, Peoples R China
通讯作者：
通讯机构：[1]Lingnan Normal Univ, Western Guangdong Characterist Biomed Engn Technol, Sch Chem & Chem Engn, Zhanjiang, Peoples R China[2]Lingnan Normal Univ, Mangrove Inst, Dept Pharmaceut Engn, Zhanjiang, Peoples R China[4]Guangzhou Univ Chinese Med, Affiliated Hosp 2, Dept Neurol, Guangzhou, Guangdong, Peoples R China[5]Guangdong Prov Hosp Chinese Med, Dept Neurol, Guangzhou, Guangdong, Peoples R China[*1]Lingnan Normal Univ, Western Guangdong Characterist Biomed Engn Technol, Sch Chem & Chem Engn, Zhanjiang 524048, Peoples R China[*2]Guangzhou Univ Chinese Med, Affiliated Hosp 2, Guangzhou 510006, Peoples R China
推荐引用方式(GB/T 7714)：
Huang Liping,Zhong Xiaoqin,Xu Yuanhang,et al.β-asarone Protects p-tau from Okadaic Acid in PC12 Cells by Activating PP2A and Involving Akt/mTOR/Beclin-1 Pathway[J].PHARMACOGNOSY MAGAZINE.2023,19(3):727-735.doi:10.1177/09731296231168743.
APA：
Huang, Liping,Zhong, Xiaoqin,Xu, Yuanhang,Deng, Minzhen&Zhou, Zhongliu.(2023).β-asarone Protects p-tau from Okadaic Acid in PC12 Cells by Activating PP2A and Involving Akt/mTOR/Beclin-1 Pathway.PHARMACOGNOSY MAGAZINE,19,(3)
MLA：
Huang, Liping,et al."β-asarone Protects p-tau from Okadaic Acid in PC12 Cells by Activating PP2A and Involving Akt/mTOR/Beclin-1 Pathway".PHARMACOGNOSY MAGAZINE 19..3(2023):727-735
