Polydatin (PD), a resveratrol (RES) glycoside, has a stronger antioxidative effect than RES. It is known that RES is an autophagic enhancer and exerts a cardioprotective effect against ischaemia/reperfusion (I/R) injury. However, the effect of PD post-treatment on myocardial I/R injury remains unclear. In the present study, we investigated the influences of PD post-treatment on myocardial I/R injury and autophagy. C57BL/6 mice underwent left coronary artery (LCA) occlusion and cultured neonatal rat cardiomyocytes (NRCs) subjected to hypoxia were treated with vehicle or PD during reperfusion or re-oxygenation. We noted that PD enhanced autophagy and decreased apoptosis during I/R or hypoxia/reoxygenation (H/R), and this effect was antagonized by co-treatment with adenovirus carrying short hairpin RNA for Beclin 1 and 3-methyladenine (3-MA), an autophagic inhibitor. Compared with vehicle-treated mice, PD-treated mice had a significantly smaller myocardial infarct size (IS) and a higher left ventricular fractional shortening (LVFS) and ejection fraction (EF), whereas these effects were partly reversed by 3-MA. Furthermore, in the PD-treated NRCs, tandem fluorescent mRFP-GFP-LC3 assay showed abundant clearance of autophagosomes with an enhanced autophagic flux, and co-treatment with Bafilomycin A1 (Baf), a lysosomal inhibitor, indicated that PD promoted the degradation of autolysosome. In addition, PD post-treatment reduced mitochondrial membrane potential and cellular reactive oxygen species (ROS) production in NRCs, and these effects were partially blocked by Baf. These findings indicate that PD post-treatment limits myocardial I/R injury by promoting autophagic flux to clear damaged mitochondria to reduce ROS and cell death.
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Corin protein expression in human renal proximal convoluted tubules as shown by brown staining in immunohistochemistry. See pp. 1655-1664 for further details. Image kindly provided by Qingyu Wu.
Research Article|
August 08 2016
Polydatin post-treatment alleviates myocardial ischaemia/reperfusion injury by promoting autophagic flux
Yuanna Ling;
Yuanna Ling
1
*Sino-Japan Collaborative Laboratory for Heart Failure Translating Medicine, Department of Cardiology, Zhujiang Hospital of Southern Medical University, No. 253, Middle Gongye Avenue, 510282 Guangzhou, China
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Guiming Chen;
Guiming Chen
1
†Department of Pathophysiology, Southern Medical University, No. 1838, Northern Guangzhou Avenue, 510515 Guangzhou, China
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Yi Deng;
Yi Deng
*Sino-Japan Collaborative Laboratory for Heart Failure Translating Medicine, Department of Cardiology, Zhujiang Hospital of Southern Medical University, No. 253, Middle Gongye Avenue, 510282 Guangzhou, China
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Huixiong Tang;
Huixiong Tang
*Sino-Japan Collaborative Laboratory for Heart Failure Translating Medicine, Department of Cardiology, Zhujiang Hospital of Southern Medical University, No. 253, Middle Gongye Avenue, 510282 Guangzhou, China
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Long Ling;
Long Ling
‡Department of Cardiology, 421 Hospital of Chinese People's Liberation Army, No. 468, Xingang Road, 510318 Guangzhou, China
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Xiaoming Zhou;
Xiaoming Zhou
§Department of Rehabilitation, the Sixth Affiliated Hospital of Sun Yat-Sen University, No. 26, Yuanchun Er Henglu, 510655 Guangzhou, China
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Xudong Song;
Xudong Song
*Sino-Japan Collaborative Laboratory for Heart Failure Translating Medicine, Department of Cardiology, Zhujiang Hospital of Southern Medical University, No. 253, Middle Gongye Avenue, 510282 Guangzhou, China
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Pingzhen Yang;
Pingzhen Yang
*Sino-Japan Collaborative Laboratory for Heart Failure Translating Medicine, Department of Cardiology, Zhujiang Hospital of Southern Medical University, No. 253, Middle Gongye Avenue, 510282 Guangzhou, China
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Yingfeng Liu;
Yingfeng Liu
*Sino-Japan Collaborative Laboratory for Heart Failure Translating Medicine, Department of Cardiology, Zhujiang Hospital of Southern Medical University, No. 253, Middle Gongye Avenue, 510282 Guangzhou, China
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Zhiliang Li;
Zhiliang Li
*Sino-Japan Collaborative Laboratory for Heart Failure Translating Medicine, Department of Cardiology, Zhujiang Hospital of Southern Medical University, No. 253, Middle Gongye Avenue, 510282 Guangzhou, China
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Cong Zhao;
Cong Zhao
*Sino-Japan Collaborative Laboratory for Heart Failure Translating Medicine, Department of Cardiology, Zhujiang Hospital of Southern Medical University, No. 253, Middle Gongye Avenue, 510282 Guangzhou, China
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Yufei Yang;
Yufei Yang
*Sino-Japan Collaborative Laboratory for Heart Failure Translating Medicine, Department of Cardiology, Zhujiang Hospital of Southern Medical University, No. 253, Middle Gongye Avenue, 510282 Guangzhou, China
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Xianbao Wang;
*Sino-Japan Collaborative Laboratory for Heart Failure Translating Medicine, Department of Cardiology, Zhujiang Hospital of Southern Medical University, No. 253, Middle Gongye Avenue, 510282 Guangzhou, China
Correspondence: Professor Aihua Chen (email [email protected]) or Dr Xianbao Wang (email [email protected]).
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Masafumi Kitakaze;
Masafumi Kitakaze
*Sino-Japan Collaborative Laboratory for Heart Failure Translating Medicine, Department of Cardiology, Zhujiang Hospital of Southern Medical University, No. 253, Middle Gongye Avenue, 510282 Guangzhou, China
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Yulin Liao;
Yulin Liao
*Sino-Japan Collaborative Laboratory for Heart Failure Translating Medicine, Department of Cardiology, Zhujiang Hospital of Southern Medical University, No. 253, Middle Gongye Avenue, 510282 Guangzhou, China
║State Key Laboratory of Organ Failure Research, Department of Cardiology, Nanfang Hospital, Southern Medical University, 510515 Guangzhou, China
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Aihua Chen
*Sino-Japan Collaborative Laboratory for Heart Failure Translating Medicine, Department of Cardiology, Zhujiang Hospital of Southern Medical University, No. 253, Middle Gongye Avenue, 510282 Guangzhou, China
Correspondence: Professor Aihua Chen (email [email protected]) or Dr Xianbao Wang (email [email protected]).
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Publisher: Portland Press Ltd
Received:
February 04 2016
Revision Received:
May 29 2016
Accepted:
June 22 2016
Accepted Manuscript online:
June 23 2016
Online ISSN: 1470-8736
Print ISSN: 0143-5221
© 2016 The Author(s). published by Portland Press Limited on behalf of the Biochemical Society
2016
Clin Sci (Lond) (2016) 130 (18): 1641–1653.
Article history
Received:
February 04 2016
Revision Received:
May 29 2016
Accepted:
June 22 2016
Accepted Manuscript online:
June 23 2016
Citation
Yuanna Ling, Guiming Chen, Yi Deng, Huixiong Tang, Long Ling, Xiaoming Zhou, Xudong Song, Pingzhen Yang, Yingfeng Liu, Zhiliang Li, Cong Zhao, Yufei Yang, Xianbao Wang, Masafumi Kitakaze, Yulin Liao, Aihua Chen; Polydatin post-treatment alleviates myocardial ischaemia/reperfusion injury by promoting autophagic flux. Clin Sci (Lond) 1 September 2016; 130 (18): 1641–1653. doi: https://doi.org/10.1042/CS20160082
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