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

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Article · Volume 19, Issue 3 · pp. 727–735

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

Liping Huang1,2, Xiaoqin Zhong3, Yuanhang Xu1, Minzhen Deng4,5, Zhongliu Zhou1,2

  1. 1School of Chemistry and Chemical Engineering, Western Guangdong Characteristic Biomedical Engineering Technology Research Center, Lingnan Normal University, Zhanjiang, China.
  2. 2Department of Pharmaceutical Engineering, Mangrove Institute, Lingnan Normal University, Zhanjiang, China.
  3. 3Department of Synopsis of Prescriptions of the Golden Chamber, The First Clinical College of Guangzhou University of Chinese Medicine, Guangzhou, Guangdong, China.
  4. 4Department of Neurology, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, Guangdong, China.
  5. 5Department of Neurology, Guangdong Provincial Hospital of Chinese Medicine, Guangzhou, Guangdong, China.

Abstract

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 β-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 β-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, Aβ42, β-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 β-asarone enhanced cell viability induced by OA in a dose-dependent manner. Moreover, compared to the OA model, p-tau, Aβ42, β-secretase, and Beclin-1 were reduced, while PP2A, p-Akt, and p-mTOR increased after treatment with β-asarone.Conclusion: All data suggested that β-asarone decreased p-tau, Aβ42, and β-secretase levels, and activated PP2A levels by inhibiting Beclin-1-dependent autophagy in OA model cells, involving Akt/mTOR/Beclin-1 pathway.

Keywords: β-asarone; tau hyperphosphorylation; okadaic acid; PC12 cell; Alzheimer’s disease

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