Berberine Protects against Hydrogen Peroxide-Induced Oxidative Damage in PC12 Cells through Activation of ERK1/2 Pathway
- *Corresponding Author:
- Zheng W
Faculty of Health Sciences
University of Macau, Taipa
E-mail: [email protected]
Received date: April 24, 2017; Accepted date: May 02, 2017; Published date: May 09, 2017
Citation: Liu L, Zeng Z, Gaur U, Fang J, Little PJ, et al. (2017) Berberine Protects against Hydrogen Peroxide-Induced Oxidative Damage in PC12 Cells through Activation of ERK1/2 Pathway. Clin Exp Pharmacol 7:236. doi: 10.4172/2161-1459.1000236
Copyright: © 2017 Liu L, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Oxidative stress is a much-recognized phenomenon linked with the progression of Neurodegenerative Diseases (NDs) due to imbalances in redox homeostasis. Increasing evidence indicates that excessive Reactive Oxygen Species (ROS), impairing the physiological functions of neurons via inducing cell apoptosis, is the main cause of NDs. The drug candidates are required that can effectively protect neurons from oxidative stress insult to slow down the process of neurodegenerative diseases. In present study, we investigated the protective effect and the underlying mechanisms of berberine (BBR, an isoquinoline alkaloid isolated from the herb Rhizoma coptidis, against oxidative damage in PC12 cells. It was found that BBR was able to suppress hydrogen peroxide (H2O2)- induced cell death in PC12 cells. Flow cytometry revealed that BBR significantly reduced the apoptosis of PC12 cells exposed to H2O2. Western blot analysis displayed that BBR stimulated the extracellular regulated ERK1/2 survival signaling, while application of PC12 cells with ERK1/2 pathway inhibitor PD98059 blocked the neuroprotective effect of BBR. These results together indicated that BBR is a potential protectant, and it protects PC12 cells against H2O2 toxicity through activated the ERK1/2 pathway.