- About this Journal ·
- Abstracting and Indexing ·
- Aims and Scope ·
- Annual Issues ·
- Article Processing Charges ·
- Author Guidelines ·
- Bibliographic Information ·
- Citations to this Journal ·
- Contact Information ·
- Editorial Board ·
- Editorial Workflow ·
- Free eTOC Alerts ·
- Publication Ethics ·
- Recently Accepted Articles ·
- Reviewers Acknowledgment ·
- Submit a Manuscript ·
- Subscription Information ·
- Table of Contents
Evidence-Based Complementary and Alternative Medicine
Volume 2013 (2013), Article ID 237207, 17 pages
Korean Red Ginseng Extract Attenuates 3-Nitropropionic Acid-Induced Huntington’s-Like Symptoms
1Department of Anatomy, College of Korean Medicine and Institute of Korean Medicine, Kyung Hee University, Seoul 130-701, Republic of Korea
2Department of Cancer Preventive Material Development and Institute of Korean Medicine, Kyung Hee University, Seoul 130-701, Republic of Korea
3Analysis Research Team, R&D Headquarters, Korea Ginseng Corporation, Daejeon 305-805, Republic of Korea
Received 15 September 2012; Revised 29 November 2012; Accepted 2 December 2012
Academic Editor: Bashar Saad
Copyright © 2013 Minhee Jang et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
- M. Damiano, L. Galvan, N. Déglon, and E. Brouillet, “Mitochondria in Huntington's disease,” Biochimica et Biophysica Acta, vol. 1802, no. 1, pp. 52–61, 2010.
- M. E. MacDonald, C. M. Ambrose, M. P. Duyao et al., “A novel gene containing a trinucleotide repeat that is expanded and unstable on Huntington's disease chromosomes,” Cell, vol. 72, no. 6, pp. 971–983, 1993.
- J. K. Ryu, S. U. Kim, and J. G. McLarnon, “Blockade of quinolinic acid-induced neurotoxicity by pyruvate is associated with inhibition of glial activation in a model of Huntington's disease,” Experimental Neurology, vol. 187, no. 1, pp. 150–159, 2004.
- Y. F. Tai, N. Pavese, A. Gerhard et al., “Imaging microglial activation in Huntington's disease,” Brain Research Bulletin, vol. 72, no. 2-3, pp. 148–151, 2007.
- J. Leegwater-Kim and J. H. J. Cha, “The paradigm of Huntington's disease: therapeutic opportunities in neurodegeneration,” NeuroRx, vol. 1, no. 1, pp. 128–138, 2004.
- M. L. Block and J. S. Hong, “Chronic microglial activation and progressive dopaminergic neurotoxicity,” Biochemical Society Transactions, vol. 35, no. 5, pp. 1127–1132, 2007.
- C. S. Lobsiger and D. W. Cleveland, “Glial cells as intrinsic components of non-cell-autonomous neurodegenerative disease,” Nature Neuroscience, vol. 10, no. 11, pp. 1355–1360, 2007.
- E. Sapp, K. B. Kegel, N. Aronin et al., “Early and progressive accumulation of reactive microglia in the Huntington disease brain,” Journal of Neuropathology and Experimental Neurology, vol. 60, no. 2, pp. 161–172, 2001.
- D. A. Simmons, M. Casale, B. Alcon, N. Pham, N. Narayan, and G. Lynch, “Ferritin accumulation in dystrophic microglia is an early event in the development of Huntington's Disease,” GLIA, vol. 55, no. 10, pp. 1074–1084, 2007.
- M. Björkqvist, E. J. Wild, J. Thiele et al., “A novel pathogenic pathway of immune activation detectable before clinical onset in Huntington's disease,” Journal of Experimental Medicine, vol. 205, no. 8, pp. 1869–1877, 2008.
- S. J. Harper and N. Wilkie, “MAPKs: new targets for neurodegeneration,” Expert Opinion on Therapeutic Targets, vol. 7, no. 2, pp. 187–200, 2003.
- M. P. Mattson and S. Camandola, “NF-κB in neuronal plasticity and neurodegenerative disorders,” Journal of Clinical Investigation, vol. 107, no. 3, pp. 247–254, 2001.
- L. Yau and P. Zahradka, “Immunodetection of activated mitogen-activated protein kinase in vascular tissues,” Molecular and Cellular Biochemistry, vol. 172, no. 1-2, pp. 59–66, 1997.
- J. J. Haddad, “N-methyl-D-aspartate (NMDA) and the regulation of mitogen-activated protein kinase (MAPK) signaling pathways: a revolving neurochemical axis for therapeutic intervention?” Progress in Neurobiology, vol. 77, no. 4, pp. 252–282, 2005.
- J. Fan, C. M. Gladding, L. Wang, L. Y. J. Zhang, and A. M. Kaufman, “P38 MAPK is involved in enhanced NMDA receptor-dependent excitotoxicity in YAC transgenic mouse model of Huntington disease,” Neurobiology of Disease, vol. 45, no. 3, pp. 999–1009, 2012.
- Y. F. Liu, D. Dorow, and J. Marshall, “Activation of MLK2-mediated signaling cascades by polyglutamine-expanded huntingtin,” Journal of Biological Chemistry, vol. 275, no. 25, pp. 19035–19040, 2000.
- T. Sugino, K. Nozaki, and N. Hashimoto, “Activation of mitogen-activated protein kinases in gerbil hippocampus with ischemic tolerance induced by 3-nitropropionic acid,” Neuroscience Letters, vol. 278, no. 1-2, pp. 101–104, 2000.
- M. Garcia, P. Vanhoutte, C. Pages, M. J. Besson, E. Brouillet, and J. Caboche, “The mitochondrial toxin 3-nitropropionic acid induces striatal neurodegeneration via a c-Jun N-terminal kinase/c-Jun module,” Journal of Neuroscience, vol. 22, no. 6, pp. 2174–2184, 2002.
- M. Garcia, D. Charvin, and J. Caboche, “Expanded huntingtin activates the C-Jun N terminal kinase/c-Jun pathway prior to aggregate formation in striatal neurons in culture,” Neuroscience, vol. 127, no. 4, pp. 859–870, 2004.
- B. L. Apostol, K. Illes, J. Pallos et al., “Mutant huntingtin alters MAPK signaling pathways in PC12 and striatal cells: ERK1/2 protects against mutant huntingtin-associated toxicity,” Human Molecular Genetics, vol. 15, no. 2, pp. 273–285, 2006.
- C. T. Chu, D. J. Levinthal, S. M. Kulich, E. M. Chalovich, and D. B. DeFranco, “Oxidative neuronal injury: the dark side of ERK1/2,” European Journal of Biochemistry, vol. 271, no. 11, pp. 2060–2066, 2004.
- M. Hetman and A. Gosdz, “Role of extracellular signal regulated kinases 1 and 2 in neuronal survival,” European Journal of Biochemistry, vol. 271, no. 11, pp. 2050–2055, 2004.
- I. Ferrer, R. Blanco, and M. Carmona, “Differential expression of active, phosphorylation-dependent MAP kinases, MAPK/ERK, SAPK/JNK and p38, and specific transcription factor substrates following quinolinic acid excitotoxicity in the rat,” Molecular Brain Research, vol. 94, no. 1-2, pp. 48–58, 2001.
- M. Gianfriddo, A. Melani, D. Turchi, M. G. Giovannini, and F. Pedata, “Adenosine and glutamate extracellular concentrations and mitogen-activated protein kinases in the striatum of Huntington transgenic mice. Selective antagonism of adenosine A2A receptors reduces transmitter outflow,” Neurobiology of Disease, vol. 17, no. 1, pp. 77–88, 2004.
- Z. H. Qin, R. W. Chen, Y. Wang, M. Nakai, D. M. Chuang, and T. N. Chase, “Nuclear factor κB nuclear translocation upregulates c-Myc and p53 expression during NMDA receptor-mediated apoptosis in rat striatum,” Journal of Neuroscience, vol. 19, no. 10, pp. 4023–4033, 1999.
- K. T. Choi, “Botanical characteristics, pharmacological effects and medicinal components of Korean Panax ginseng C A Meyer,” Acta Pharmacologica Sinica, vol. 29, no. 9, pp. 1109–1118, 2008.
- S. Shibata, M. Fujita, H. Itokawa, O. Tanaka, and T. Ishii, “Studies on the constituents of Japanese and Chinese crude drugs. Xi. Panaxadiol, a Sapogenin of Ginseng Roots,” Chemical & Pharmaceutical Bulletin, vol. 11, pp. 759–761, 1963.
- C. Xiaoguang, L. Hongyan, L. Xiaohong et al., “Cancer chemopreventive and therapeutic activities of red ginseng,” Journal of Ethnopharmacology, vol. 60, no. 1, pp. 71–78, 1998.
- S. H. Oh and B. H. Lee, “A ginseng saponin metabolite-induced apoptosis in HepG2 cells involves a mitochondria-mediated pathway and its downstream caspase-8 activation and Bid cleavage,” Toxicology and Applied Pharmacology, vol. 194, no. 3, pp. 221–229, 2004.
- H. I. Jang and H. M. Shin, “Wild Panax ginseng (Panax ginseng C.A. Meyer) protects against methotrexate-induced cell regression by enhancing the immune response in RAW 264.7 macrophages,” American Journal of Chinese Medicine, vol. 38, no. 5, pp. 949–960, 2010.
- K. Radad, G. Gille, L. Liu, and W. D. Rausch, “Use of ginseng in medicine with emphasis on neurodegenerative disorders,” Journal of Pharmacological Sciences, vol. 100, no. 3, pp. 175–186, 2006.
- I.-H. Cho, “Efects of Panax ginseng in neurodegenerative diseases,” Journal of Ginseng Research, vol. 36, no. 4, pp. 342–353, 2012.
- C. G. Benishin, “Actions of ginsenoside Rb1 on choline uptake in central cholinergic nerve endings,” Neurochemistry International, vol. 21, no. 1, pp. 1–5, 1992.
- M. Rudakewich, F. Ba, and C. G. Benishin, “Neurotrophic and neuroprotective actions of ginsenosides Rb1and Rg1,” Planta Medica, vol. 67, no. 6, pp. 533–537, 2001.
- H. Y. Cha, J. H. Park, J. T. Hong et al., “Anxiolytic-like effects of ginsenosides on the elevated plus-maze model in mice,” Biological and Pharmaceutical Bulletin, vol. 28, no. 9, pp. 1621–1625, 2005.
- X. Wang, S. Zhu, M. Drozda et al., “Minocycline inhibits caspase-independent and -dependent mitochondrial cell death pathways in models of Huntington's disease,” Proceedings of the National Academy of Sciences of the United States of America, vol. 100, no. 18, pp. 10483–10487, 2003.
- J. H. Kim, S. Kim, I. S. Yoon et al., “Protective effects of ginseng saponins on 3-nitropropionic acid-induced striatal degeneration in rats,” Neuropharmacology, vol. 48, no. 5, pp. 743–756, 2005.
- J. Wu, H. K. Jeong, S. E. Bulin, S. W. Kwon, J. H. Park, and I. Bezprozvanny, “Ginsenosides protect striatal neurons in a cellular model of Huntington's disease,” Journal of Neuroscience Research, vol. 87, no. 8, pp. 1904–1912, 2009.
- Z. A. Shah, R. A. Gilani, P. Sharma, and S. B. Vohora, “Cerebroprotective effect of Korean ginseng tea against global and focal models of ischemia in rats,” Journal of Ethnopharmacology, vol. 101, no. 1–3, pp. 299–307, 2005.
- G. Q. Zheng, W. Cheng, Y. Wang et al., “Ginseng total saponins enhance neurogenesis after focal cerebral ischemia,” Journal of Ethnopharmacology, vol. 133, no. 2, pp. 724–728, 2011.
- J. S. Jung, J. A. Shin, E. M. Park et al., “Anti-inflammatory mechanism of ginsenoside Rh1 in lipopolysaccharide- stimulated microglia: critical role of the protein kinase A pathway and hemeoxygenase-1 expression,” Journal of Neurochemistry, vol. 115, no. 6, pp. 1668–1680, 2010.
- J. S. Park, E. M. Park, D. H. Kim et al., “Anti-inflammatory mechanism of ginseng saponins in activated microglia,” Journal of Neuroimmunology, vol. 209, no. 1-2, pp. 40–49, 2009.
- J. Zhu, Y. Jiang, L. Wu, T. Lu, G. Xu, and X. Liu, “Suppression of local inflammation contributes to the neuroprotective effect of ginsenoside Rb1 in rats with cerebral ischemia,” Neuroscience, vol. 202, pp. 342–351, 2012.
- H. Y. Son, H. S. Han, H. W. Jung, and Y. K. Park, “Panax notoginseng attenuates the infarct volume in rat ischemic brain and the inflammatory response of microglia,” Journal of Pharmacological Sciences, vol. 109, no. 3, pp. 368–379, 2009.
- Korea Food and Drug Administration, Korea Food and Drug Administration, Korea Food Code, Mun-Young, Seoul, Republic of Korea, 2007.
- Q. Y. Huang, C. Wei, L. Yu et al., “Adenosine A2A receptors in bone marrow-derived cells but not in forebrain neurons are important contributors to 3-nitropropionic acid-induced striatal damage as revealed by cell-type-selective inactivation,” Journal of Neuroscience, vol. 26, no. 44, pp. 11371–11378, 2006.
- P. O. Fernagut, E. Diguet, N. Stefanova et al., “Subacute systemic 3-nitropropionic acid intoxication induces a distinct motor disorder in adult C57Bl/6 mice: behavioural and histopathological characterisation,” Neuroscience, vol. 114, no. 4, pp. 1005–1017, 2002.
- K. J. B. Franklin and G. Paxions, The Mouse Brain in Stereotaxic Coordinates, Elsevier Academic Press, San Diego, Calif, USA, 2008.
- I. H. Cho, J. Hong, E. C. Suh et al., “Role of microglial IKKβ in kainic acid-induced hippocampal neuronal cell death,” Brain, vol. 131, no. 11, pp. 3019–3033, 2008.
- K. J. Livak and T. D. Schmittgen, “Analysis of relative gene expression data using real-time quantitative PCR and the 2-ΔΔCT method,” Methods, vol. 25, no. 4, pp. 402–408, 2001.
- C. Mestre, T. Pelissier, J. Fialip, G. Wilcox, and A. Eschalier, “A method to perform direct transcutaneous intrathecal injection in rats,” Journal of Pharmacological and Toxicological Methods, vol. 32, no. 4, pp. 197–200, 1994.
- M. Jang, H.-S. Jung, S.-H. Kim, and I.-H. Cho, “Ethyl pyruvate attenuates formalin-induced inflammatory nociception by inhibiting neuronal ERK phosphorylation,” Molecular Pain, vol. 8, article 40, 2012.
- X. C. Chen, Y. C. Zhou, Y. Chen, Y. G. Zhu, F. Fang, and L. M. Chen, “Ginsenoside Rg1 reduces MPTP-induced substantia nigra neuron loss by suppressing oxidative stress,” Acta Pharmacologica Sinica, vol. 26, no. 1, pp. 56–62, 2005.
- K. L. Ge, W. F. Chen, J. X. Xie, and M. S. Wong, “Ginsenoside Rg1 protects against 6-OHDA-induced toxicity in MES23.5 cells via Akt and ERK signaling pathways,” Journal of Ethnopharmacology, vol. 127, no. 1, pp. 118–123, 2010.
- M. Gu, M. T. Gash, V. M. Mann, F. Javoy-Agid, J. M. Cooper, and A. H. V. Schapira, “Mitochondrial defect in Huntington's disease caudate nucleus,” Annals of Neurology, vol. 39, no. 3, pp. 385–389, 1996.
- S. E. Browne, A. C. Bowling, U. MacGarvey et al., “Oxidative damage and metabolic dysfunction in huntington's disease: selective vulnerability of the basal ganglia,” Annals of Neurology, vol. 41, no. 5, pp. 646–653, 1997.
- S. J. Tabrizi, M. W. J. Cleeter, J. Xuereb, J.-W. Taanman, J. M. Cooper, and A. H. V. Schapira, “Biochemical abnormalities and excitotoxicity in Huntington's disease brain,” Annals of Neurology, vol. 45, no. 1, pp. 25–32, 1999.
- A. V. Panov, C. A. Gutekunst, B. R. Leavitt et al., “Early mitochondrial calcium defects in Huntington's disease are a direct effect of polyglutamines,” Nature Neuroscience, vol. 5, no. 8, pp. 731–736, 2002.
- M. F. Beal, “Mitochondria take center stage in aging and neurodegeneration,” Annals of Neurology, vol. 58, no. 4, pp. 495–505, 2005.
- E. Brouillet, C. Jacquard, N. Bizat, and D. Blum, “3-Nitropropionic acid: a mitochondrial toxin to uncover physiopathological mechanisms underlying striatal degeneration in Huntington's disease,” Journal of Neurochemistry, vol. 95, no. 6, pp. 1521–1540, 2005.
- M. Chen, V. O. Ona, M. Li et al., “Minocycline inhibits caspase-1 and caspase-3 expression and delays mortality in a transgenic mouse model of Huntington disease,” Nature Medicine, vol. 6, no. 7, pp. 797–801, 2000.
- C. C. Hsieh and J. Papaconstantinou, “The effect of aging on p38 signaling pathway activity in the mouse liver and in response to ROS generated by 3-nitropropionic acid,” Mechanisms of Ageing and Development, vol. 123, no. 11, pp. 1423–1435, 2002.
- C. C. Hsieh, J. I. Rosenblatt, and J. Papaconstantinou, “Age-associated changes in SAPK/JNK and p38 MAPK signaling in response to the generation of ROS by 3-nitropropionic acid,” Mechanisms of Ageing and Development, vol. 124, no. 6, pp. 733–746, 2003.
- A. Kulisz, N. Chen, N. S. Chandel, Z. Shao, and P. T. Schumacker, “Mitochondrial ROS initiate phosphorylation of p38 MAP kinase during hypoxia in cardiomyocytes,” American Journal of Physiology, vol. 282, no. 6, pp. L1324–L1329, 2002.
- P. Juo, C. J. Kuo, S. E. Reynolds et al., “Fas activation of the p38 mitogen-activated protein kinase signalling pathway requires ICE/CED-3 family proteases,” Molecular and Cellular Biology, vol. 17, no. 1, pp. 24–35, 1997.
- I. Bezprozvanny and M. R. Hayden, “Deranged neuronal calcium signaling and Huntington disease,” Biochemical and Biophysical Research Communications, vol. 322, no. 4, pp. 1310–1317, 2004.
- E. Cattaneo and P. Calabresi, “Mutant huntingtin goes straight to the heart,” Nature Neuroscience, vol. 5, no. 8, pp. 711–712, 2002.
- S. Camandola and M. P. Mattson, “NF-κB as a therapeutic target in neurodegenerative diseases,” Expert Opinion on Therapeutic Targets, vol. 11, no. 2, pp. 123–132, 2007.
- R. Malek, K. K. Borowicz, M. Jargiello, and S. J. Czuczwar, “Role of nuclear factor kappaB in the central nervous system,” Pharmacological Reports, vol. 59, no. 1, pp. 25–33, 2007.
- D. F. Cechetto, “Role of nuclear factor kappa B in neuropathological mechanisms,” Progress in Brain Research, vol. 132, pp. 391–404, 2001.