Volume 46, Issue 3 e13820
SPECIAL ISSUE ORIGINAL ARTICLE

Piceatannol alleviate ROS-mediated PC-12 cells damage and mitochondrial dysfunction through SIRT3/FOXO3a signaling pathway

Wei Yang

Wei Yang

China-Canada Joint Lab of Food Nutrition and Health (Beijing), Beijing Technology and Business University (BTBU), Beijing, China

College of Basic Science, Tianjin Agricultural University, Tianjin, China

Contribution: Writing - original draft

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Yu Wang

Yu Wang

China-Canada Joint Lab of Food Nutrition and Health (Beijing), Beijing Technology and Business University (BTBU), Beijing, China

Contribution: Data curation

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Yiming Hao

Yiming Hao

China-Canada Joint Lab of Food Nutrition and Health (Beijing), Beijing Technology and Business University (BTBU), Beijing, China

Contribution: Validation

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Ziyuan Wang

Ziyuan Wang

China-Canada Joint Lab of Food Nutrition and Health (Beijing), Beijing Technology and Business University (BTBU), Beijing, China

Contribution: Writing - review & editing

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Jie Liu

Corresponding Author

Jie Liu

China-Canada Joint Lab of Food Nutrition and Health (Beijing), Beijing Technology and Business University (BTBU), Beijing, China

Correspondence

Jie Liu and Jing Wang, China-Canada Joint Lab of Food Nutrition and Health (Beijing), Beijing Technology and Business University (BTBU), Beijing, China.

Email: [email protected] (J. L.) and [email protected] (J. W.)

Contribution: Project administration

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Jing Wang

Corresponding Author

Jing Wang

China-Canada Joint Lab of Food Nutrition and Health (Beijing), Beijing Technology and Business University (BTBU), Beijing, China

Correspondence

Jie Liu and Jing Wang, China-Canada Joint Lab of Food Nutrition and Health (Beijing), Beijing Technology and Business University (BTBU), Beijing, China.

Email: [email protected] (J. L.) and [email protected] (J. W.)

Contribution: Project administration

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First published: 16 June 2021
Citations: 16

Abstract

Oxidative stress-associated mitochondrial dysfunction has been identified as a major mechanism in multiple neurodegenerative diseases. This study aims to investigate the cytoprotective effects of piceatannol on ROS-mediated PC-12 cells damage and related mitochondrial dysfunction. Piceatannol treatment could significantly attenuate PC-12 cells oxidative damage and ROS-mediated cells apoptosis. Moreover, pretreatment with piceatannol effectively decreased mitochondrial membrane depolarization, cleaved-caspase 3, and increased Bcl-2 and Bcl-2/Bax compared with control H2O2 group. Meanwhile, piceatannol treatment improved mitochondrial respiration function which led to an enhancement in the maximal respiration and spare respiratory capacity. Further mechanisms analysis showed that the protein expression of SIRT3 and its downstream protein FOXO3a were significantly increased after piceatannol addition in a dose-dependent manner. Whereas the cytoprotective role of piceatannol was markedly abolished by the SIRT3 inhibitor 3-TYP, suggesting that SIRT3/FOXO3a signaling pathway played a vital role in mediating the neuronal cytoprotective effects of piceatannol.

Practical applications

The results of our study provide a novel insight that piceatannol could be potentially used as a promising bioactive component against oxidative damage and neurocyte apoptosis. The findings may provide theoretical basis for brain health of piceatannol consumption in some extent.

CONFLICT OF INTEREST

The authors declare that there are no conflicts of interest.

DATA AVAILABILITY STATEMENT

The data that support the findings of this study are available from the corresponding author upon reasonable request.

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