Berberine protects 6-hydroxydopamine-induced human dopaminergic neuronal cell death through the induction of heme oxygenase-1

被引：74
作者：
Bae, Jinbum [1 ]
Lee, Danbi [1 ]
Kim, Yun Kyu [1 ]
Gil, Minchan [1 ,2 ]
Lee, Joo-Yong [1 ,2 ]
Lee, Kyung Jin [1 ,2 ]
机构：
[1] Asan Med Ctr, Asan Inst Life Sci, Seoul 138736, South Korea
[2] Univ Ulsan, Dept Med, Coll Med, Seoul 138736, South Korea
来源：
MOLECULES AND CELLS | 2013年 / 35卷 / 02期
基金：
新加坡国家研究基金会;
关键词：
berberine; heme oxygenase-1; neuroprotection; NF-E2 related factor; phosphatidylinositol; 3-kinase; RESPONSE ELEMENT PATHWAY; OXIDATIVE STRESS; TRANSCRIPTION FACTOR; 15-DEOXY-DELTA(12,14)-PROSTAGLANDIN J(2); PARKINSONS-DISEASE; SIGNALING PATHWAYS; IN-VITRO; NRF2; EXPRESSION; ACTIVATION;
D O I：
10.1007/s10059-013-2298-5
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
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 neuronal 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-OHDAinduced generation of reactive oxygen species (ROS), caspase-3 activation, and subsequent cell death. BBR also upregulated heme oxygenase-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.
引用
收藏
页码：151 / 157
页数：7
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