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Mol. Cells 2013; 35(2): 151-157

Published online February 28, 2013

https://doi.org/10.1007/s10059-013-2298-5

© The Korean Society for Molecular and Cellular Biology

Berberine Protects 6-Hydroxydopamine-Induced Human Dopaminergic Neuronal Cell Death through the Induction of Heme Oxygenase-1

Jinbum Bae, Danbi Lee, Yun Kyu Kim1, Minchan Gil, Joo-Yong Lee, and Kyung Jin Lee

1Asan Institute for Life Sciences, Asan Medical Center, Seoul 138-736, Korea, 2Department of Medicine, University of Ulsan College of Medicine, Seoul 138-736, Korea

Received: November 21, 2012; Revised: December 18, 2012; Accepted: December 21, 2012

Abstract

Berberine (BBR) is one of the major alkaloids and has been reported to have a variety of pharmacologic effects, including inhibition of cell cycle progression. Here, we investigated the mechanisms of BBR protection of neu-ronal cells from cell death induced by the Parkinson’s disease-related neurotoxin 6-hydroxydopamine (6-OHDA). Pretreatment of SH-SY5Y cells with BBR significantly reduced 6-OHDA-induced generation of reactive oxygen species (ROS), caspase-3 activation, and subsequent cell death. BBR also upregulated heme oxy-genase-1 (HO-1) expression, which conferred protection against 6-OHDA-induced dopaminergic neuron injury and besides, effect of BBR on HO-1 was reversed by siRNA-Nrf2. Furthermore, BBR induced PI3K/ Akt and p38 activation, which are involved in the induction of Nrf2 expression and neuroprotection. These results suggest that BBR may be useful as a therapeutic agent for the treatment of dopaminergic neuronal diseases.

Keywords berberine, heme oxygenase-1, neuroprotection, NF-E2 related factor, phosphatidylinositol 3-kinase

Article

Research Article

Mol. Cells 2013; 35(2): 151-157

Published online February 28, 2013 https://doi.org/10.1007/s10059-013-2298-5

Copyright © The Korean Society for Molecular and Cellular Biology.

Berberine Protects 6-Hydroxydopamine-Induced Human Dopaminergic Neuronal Cell Death through the Induction of Heme Oxygenase-1

Jinbum Bae, Danbi Lee, Yun Kyu Kim1, Minchan Gil, Joo-Yong Lee, and Kyung Jin Lee

1Asan Institute for Life Sciences, Asan Medical Center, Seoul 138-736, Korea, 2Department of Medicine, University of Ulsan College of Medicine, Seoul 138-736, Korea

Received: November 21, 2012; Revised: December 18, 2012; Accepted: December 21, 2012

Abstract

Berberine (BBR) is one of the major alkaloids and has been reported to have a variety of pharmacologic effects, including inhibition of cell cycle progression. Here, we investigated the mechanisms of BBR protection of neu-ronal cells from cell death induced by the Parkinson’s disease-related neurotoxin 6-hydroxydopamine (6-OHDA). Pretreatment of SH-SY5Y cells with BBR significantly reduced 6-OHDA-induced generation of reactive oxygen species (ROS), caspase-3 activation, and subsequent cell death. BBR also upregulated heme oxy-genase-1 (HO-1) expression, which conferred protection against 6-OHDA-induced dopaminergic neuron injury and besides, effect of BBR on HO-1 was reversed by siRNA-Nrf2. Furthermore, BBR induced PI3K/ Akt and p38 activation, which are involved in the induction of Nrf2 expression and neuroprotection. These results suggest that BBR may be useful as a therapeutic agent for the treatment of dopaminergic neuronal diseases.

Keywords: berberine, heme oxygenase-1, neuroprotection, NF-E2 related factor, phosphatidylinositol 3-kinase

Mol. Cells
Nov 30, 2022 Vol.45 No.11, pp. 763~867
COVER PICTURE
Naive (cyan) and axotomized (magenta) retinal ganglion cell axons in Xenopus tropicalis (Choi et al., pp. 846-854).

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