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Original Research ARTICLE Provisionally accepted The full-text will be published soon. Notify me

Front. Pharmacol. | doi: 10.3389/fphar.2018.01121

Berberine ameliorates high glucose-induced cardiomyocyte injury via AMPK signaling activation to stimulate mitochondrial biogenesis and restore autophagic flux

Weijian Hang1, 2, Benhong He3, Jiehui Chen1, Liangtao Xia1, Bin Wen1, Tao Liang1, Xu Wang1, Qianying Zhang1, Yue Wu1,  Qingjie Chen1, 4* and  Juan Chen1, 5, 6*
  • 1Department of Biochemistry and Molecular Biology, Tongji Medical College, Huazhong University of Science and Technology, China
  • 2Hubei Key Laboratory of Genetics and Molecular Mechanisms of Cardiological Disorders, Huazhong University of Science and Technology, China
  • 3Department of Cardiology, Lichuan People's Hospital, China
  • 4School of Basic Medicine, Hubei University of Chinese Medicine, China
  • 5Institute for Brain Research, Huazhong University of Science and Technology, China
  • 6Key Laboratory of Ministry of Education for Neurological Disorders, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, China

Background Type II diabetes (T2D) induced cardiomyocyte hypertrophy is closely linked to the impairment of mitochondrial function. Berberine has been shown to promising effect for hypoglycemia in type II diabetes models. High Glucose induced cardiomyocyte hypertrophy in vitro has been reported. The present study investigated the protective effect and the underlying mechanism of berberine on high glucose-induced H9C2 cell line.
Methods High glucose-induced H9C2 cell line was used to mimic the hyperglycemia resulting in cardiomyocyte hypertrophy. Berberine was used to rescue in this model and explore the mechanism in it. Confocal microscopy, Immunofluorescence, RT-PCR and western blot analysis was performed to evaluate the protective effects of berberine in high glucose-induced H9C2 cell line.
Results Berberine dramatically alleviated hypertrophy of H9C2 cell line and significantly ameliorated mitochondrial function by rectified the imbalance of fusion and fission in mitochondrial dynamic. Furthermore, berberine further promoted mitogenesis and cleared the damaged mitochondria via mitophagy. In addition, berberine also restored autophagic flux in high glucose-induced cardiomyocyte injury via AMPK signaling pathway activation.
Conclusion Berberine ameliorates high glucose-induced cardiomyocyte injury via AMPK signaling pathway activation to stimulate mitochondrial biogenesis and restore autophagic flux in H9C2 cell line.

Keywords: Berberine (BBR), cardiomyocyte hypertrophy, mitochondrial, high glucose, fragmentation, Diabetes Mellitus

Received: 29 Jun 2018; Accepted: 13 Sep 2018.

Edited by:

Li-Long Pan, Fudan University, China

Reviewed by:

Lihong Chen, Dalian Medical University, China
Soon Yew Tang, University of Pennsylvania, United States  

Copyright: © 2018 Hang, He, Chen, Xia, Wen, Liang, Wang, Zhang, Wu, Chen and Chen. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence:
Dr. Qingjie Chen, Department of Biochemistry and Molecular Biology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei Province, China, chenqingjie8858@163.com
Prof. Juan Chen, Department of Biochemistry and Molecular Biology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei Province, China, chenjuanlinda69@163.com