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本文引用的文献

1
Omega-3 polyunsaturated fatty acid has an anti-oxidant effect via the Nrf-2/HO-1 pathway in 3T3-L1 adipocytes.ω-3 多不饱和脂肪酸通过 Nrf-2/HO-1 通路在 3T3-L1 脂肪细胞中发挥抗氧化作用。
Biochem Biophys Res Commun. 2013 Jan 4;430(1):225-30. doi: 10.1016/j.bbrc.2012.10.115. Epub 2012 Nov 3.
2
Heme oxygenase-1: an important therapeutic target for protecting against myocardial ischemia and reperfusion injury.血红素加氧酶-1：预防心肌缺血再灌注损伤的重要治疗靶点。
Int J Cardiol. 2013 Jul 31;167(2):587-8. doi: 10.1016/j.ijcard.2012.09.225. Epub 2012 Oct 18.
3
Oxidative stress suppression by luteolin-induced heme oxygenase-1 expression.木樨草素诱导血红素氧合酶-1 表达抑制氧化应激。
Toxicol Appl Pharmacol. 2012 Dec 1;265(2):229-40. doi: 10.1016/j.taap.2012.10.002. Epub 2012 Oct 7.
4
Anti-apoptotic and anti-inflammatory effect of Piperine on 6-OHDA induced Parkinson's rat model.胡椒碱对 6-OHDA 诱导的帕金森病大鼠模型的抗凋亡和抗炎作用。
J Nutr Biochem. 2013 Apr;24(4):680-7. doi: 10.1016/j.jnutbio.2012.03.018. Epub 2012 Jul 20.
5
Berberine sensitizes mutliple human cancer cells to the anticancer effects of doxorubicin in vitro.小檗碱在体外使多种人类癌细胞对阿霉素的抗癌作用敏感。
Oncol Lett. 2012 Jun;3(6):1263-1267. doi: 10.3892/ol.2012.644. Epub 2012 Mar 14.
6
Berberine activates Nrf2 nuclear translocation and protects against oxidative damage via a phosphatidylinositol 3-kinase/Akt-dependent mechanism in NSC34 motor neuron-like cells.小檗碱通过磷酸肌醇 3-激酶/ Akt 依赖性机制激活 Nrf2 核易位，保护 NSC34 运动神经元样细胞免受氧化损伤。
Eur J Pharm Sci. 2012 Aug 15;46(5):415-25. doi: 10.1016/j.ejps.2012.03.004. Epub 2012 Mar 24.
7
PI3K and ERK/Nrf2 pathways are involved in oleanolic acid-induced heme oxygenase-1 expression in rat vascular smooth muscle cells.PI3K 和 ERK/Nrf2 通路参与齐墩果酸诱导的大鼠血管平滑肌细胞血红素加氧酶-1 的表达。
J Cell Biochem. 2011 Jun;112(6):1524-31. doi: 10.1002/jcb.23065.
8
Biomarkers of cell damage induced by oxidative stress in Parkinson's disease and related models.帕金森病及相关模型中氧化应激诱导的细胞损伤生物标志物。
Cent Nerv Syst Agents Med Chem. 2010 Dec 1;10(4):278-86. doi: 10.2174/187152410793429719.
9
Targeting heme oxygenase-1 for neuroprotection and neuroinflammation in neurodegenerative diseases.针对神经退行性疾病中的血红素加氧酶-1 进行神经保护和神经炎症治疗。
Curr Drug Targets. 2010 Dec;11(12):1517-31. doi: 10.2174/1389450111009011517.
10
Ginsenoside Rb1 protects against 6-hydroxydopamine-induced oxidative stress by increasing heme oxygenase-1 expression through an estrogen receptor-related PI3K/Akt/Nrf2-dependent pathway in human dopaminergic cells.人参皂苷Rb1通过雌激素受体相关的PI3K/Akt/Nrf2依赖性途径增加血红素加氧酶-1的表达，从而保护人多巴胺能细胞免受6-羟基多巴胺诱导的氧化应激。
Toxicol Appl Pharmacol. 2010 Jan 1;242(1):18-28. doi: 10.1016/j.taap.2009.09.009. Epub 2009 Sep 23.

黄连素通过诱导血红素加氧酶-1保护6-羟基多巴胺诱导的人多巴胺能神经元细胞死亡。

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

作者信息

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

机构信息

Asan Institute for Life Sciences, Asan Medical Center, Seoul 138-736, Korea.

出版信息

Mol Cells. 2013 Feb;35(2):151-7. doi: 10.1007/s10059-013-2298-5. Epub 2013 Jan 16.

DOI:10.1007/s10059-013-2298-5
PMID:23329300
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3887902/
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 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.

摘要

黄连素（BBR）是主要生物碱之一，据报道具有多种药理作用，包括抑制细胞周期进程。在此，我们研究了黄连素保护神经元细胞免受帕金森病相关神经毒素6-羟基多巴胺（6-OHDA）诱导的细胞死亡的机制。用黄连素预处理SH-SY5Y细胞可显著减少6-OHDA诱导的活性氧（ROS）生成、半胱天冬酶-3激活及随后的细胞死亡。黄连素还上调了血红素加氧酶-1（HO-1）的表达，这赋予了对6-OHDA诱导的多巴胺能神经元损伤的保护作用，此外，黄连素对HO-1的作用被siRNA-Nrf2逆转。此外，黄连素诱导PI3K/Akt和p38激活，这参与了Nrf2表达的诱导和神经保护。这些结果表明，黄连素可能作为治疗多巴胺能神经元疾病的治疗剂。