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http://dx.doi.org/10.1016/j.jgr.2018.02.003

Korean ginseng extract ameliorates abnormal immune response through the regulation of inflammatory constituents in Sprague Dawley rat subjected to environmental heat stress  

Song, Ji-Hyeon (Department of Food Science and Biotechnology, College of Life Science, CHA University)
Kim, Kui-Jin (Department of Food Science and Biotechnology, College of Life Science, CHA University)
Choi, Seo-Yun (Department of Food Science and Biotechnology, College of Life Science, CHA University)
Koh, Eun-Jeong (Department of Food Science and Biotechnology, College of Life Science, CHA University)
Park, JongDae (Central Research Institute, Korean Ginseng Research Co., LTD.)
Lee, Boo-Yong (Department of Food Science and Biotechnology, College of Life Science, CHA University)
Publication Information
Journal of Ginseng Research / v.43, no.2, 2019 , pp. 252-260 More about this Journal
Abstract
Background: Increases in the average global temperature cause heat stress-induced disorders by disrupting homeostasis. Excessive heat stress triggers an imbalance in the immune system; thus protection against heat stress is important to maintain immune homeostasis. Korean ginseng (Panax ginseng Meyer) has been used as a herbal medicine and displays beneficial biological properties. Methods: We investigated the protective effects of Korean ginseng extracts (KGEs) against heat stress in a rat model. Following acclimatization for 1 week, rats were housed at room temperature for 2 weeks and then exposed to heat stress ($40^{\circ}C$/2 h/day) for 4 weeks. Rats were treated with three KGEs from the beginning of the second week to the end of the experiment. Results: Heat stress dramatically increased secretion of inflammatory factors, and this was significantly reduced in the KGE-treated groups. Levels of inflammatory factors such as heat shock protein 70, interleukin 6, inducible nitric oxide synthase, and tumor necrosis factor-alpha were increased in the spleen and muscle upon heat stress. KGEs inhibited these increases by down-regulating heat shock protein 70 and the associated nuclear $factor-{\kappa}B$ and mitogen-activated protein kinase signaling pathways. Consequently, KGEs suppressed activation of T-cells and B-cells. Conclusion: KGEs suppress the immune response upon heat stress and decrease the production of inflammatory cytokines in muscle and spleen. We suggest that KGEs protect against heat stress by inhibiting inflammation and maintaining immune homeostasis.
Keywords
Heat stress; Immune response; Inflammation; Korean ginseng extracts; Sprague Dawley rats;
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1 Pockley AG. Heat shock proteins, inflammation, and cardiovascular disease. Circulation 2002;105(8):1012-7.   DOI
2 Knochel JP. Heat stroke and related heat stress disorders. Dis Mon 1989;35(5): 301-77. PubMed PMID: 2653754.
3 Woo J, Iyer S, Cornejo M-C, Mori N, Gao L, Sipos I, Maines M, Buelow R. Stress protein-induced immunosuppression: inhibition of cellular immune effector functions following overexpression of haem oxygenase (HSP 32). Transpl Immunol 1998;6(2):84-93.   DOI
4 Choi S-Y, Kim K-J, Song J-H, Lee B-Y. Ginsenoside Rg5 prevents apoptosis by modulating heme-oxygenase-1/nuclear factor E2-related factor 2 signaling and alters the expression of cognitive impairment-associated genes in thermal stress-exposed HT22 cells. J Ginseng Res 2018;42:225-8.   DOI
5 Nathan C. Points of control in inflammation. Nature 2002;420(6917):846-52. https://doi.org/10.1038/nature01320. PubMed PMID: 12490957.   DOI
6 Grivennikov SI, Greten FR, Karin M. Immunity, inflammation, and cancer. Cell 2010;140(6):883-99. https://doi.org/10.1016/j.cell.2010.01.025. PubMed PMID: 20303878; PubMed Central PMCID: PMCPMC2866629.   DOI
7 Yuan H-D, Kim JT, Kim SH, Chung SH. Ginseng and diabetes: the evidences from in vitro, animal and human studies. J Ginseng Res 2012;36(1):27.   DOI
8 Putics A, Vegh EM, Csermely P, Soti C. Resveratrol induces the heat-shock response and protects human cells from severe heat stress. Antioxid Redox Signal 2008;10(1):65-76.   DOI
9 Kim K-J, Yoon K-Y, Hong H-D, Lee B-Y. Role of the red ginseng in defense against the environmental heat stress in Sprague Dawley rats. Molecules 2015;20(11):20240-53.   DOI
10 Koh E-J, Kim K-J, Choi J, Jeon HJ, Seo M-J, Lee B-Y. Ginsenoside Rg1 suppresses early stage of adipocyte development via activation of C/EBP homologous protein-10 in 3T3-L1 and attenuates fat accumulation in high fat diet-induced obese zebrafish. J Ginseng Res 2017;41(1):23-30.   DOI
11 Kang S, Min H. Ginseng, the 'immunity boost': the effects of Panax ginseng on immune system. J Ginseng Res 2012;36(4):354.   DOI
12 Somensi N, Brum PO, de Miranda Ramos V, Gasparotto J, Zanotto-Filho A, Rostirolla DC, da Silva Morrone M, Moreira JCF, Pens Gelain D. Extracellular HSP70 activates ERK1/2, NF-kB and pro-inflammatory gene transcription through binding with RAGE in A549 human lung cancer cells. Cell Physiol Biochem 2017;42(6):2507-22. https://doi.org/10.1159/000480213. PubMed PMID: 28848092.   DOI
13 Lee B-Y, Kim E-J, Park D-J, Hong S-I, Chun H-S. Composition of saponin and free sugar of some white ginsengs with processing conditions. Korean J Food Sci Technol 1996;28(5):922-7.
14 Kim S-N, Kang S-J. Effects of black ginseng (9 times-steaming ginseng) on hypoglycemic action and changes in the composition of ginsenosides on the steaming process. Korean J Food Sci Technol 2009;41(1):77-81.
15 Lewis S, Donkin M, Depledge M. Hsp70 expression in Enteromorpha intestinalis (Chlorophyta) exposed to environmental stressors. Aquat Toxicol 2001;51(3): 277-91.   DOI
16 Theriault JR, Adachi H, Calderwood SK. Role of scavenger receptors in the binding and internalization of heat shock protein 70. J Immunol 2006;177(12):8604-11.   DOI
17 Zheng Z, Kim JY, Ma H, Lee JE, Yenari MA. Anti-inflammatory effects of the 70 kDa heat shock protein in experimental stroke. J Cereb Blood Flow Metab 2008;28(1):53-63.   DOI
18 Nover L, Scharf K-D. Heat stress proteins and transcription factors. Cell Mol Life Sci 1997;53(1):80-103.   DOI
19 Becker T, Hartl F-U, Wieland F. CD40, an extracellular receptor for binding and uptake of Hsp70-peptide complexes. J Cell Biol 2002;158(7):1277-85.   DOI
20 Kawai T, Akira S. Signaling to NF-${\kappa}B$ by Toll-like receptors. Trends Mol Med 2007;13(11):460-9.   DOI
21 Gilmore TD. Introduction to NF-${\kappa}B$: players, pathways, perspectives. Oncogene 2006;25(51):6680-4.   DOI
22 Sakurai H. Targeting of TAK1 in inflammatory disorders and cancer. Trends Pharmacol Sci 2012;33(10):522-30.   DOI
23 Bennouna S, Bliss SK, Curiel TJ, Denkers EY. Cross-talk in the innate immune system: neutrophils instruct recruitment and activation of dendritic cells during microbial infection. J Immunol 2003;171(11):6052-8.   DOI
24 Iwasaki A, Medzhitov R. Regulation of adaptive immunity by the innate immune system. Science 2010;327(5963):291-5.   DOI
25 Boyman O, Sprent J. The role of interleukin-2 during homeostasis and activation of the immune system. Nature Rev Immunol 2012;12(3):180-90.   DOI
26 Curtsinger JM, Schmidt CS, Mondino A, Lins DC, Kedl RM, Jenkins MK, Mescher MF. Inflammatory cytokines provide a third signal for activation of naive CD4+ and CD8+ T cells. J Immunol 1999;162(6):3256-62.
27 Gasteiger G, Kastenmuller W. Foxp3+ regulatory T-cells and IL-2: the Moirai of T-cell fates? Front Immunol 2012;3.
28 Sorensen JG, Nielsen MM, Kruhoffer M, Justesen J, Loeschcke V. Full genome gene expression analysis of the heat stress response in Drosophila melanogaster. Cell Stress Chaperones 2005;10(4):312-28.   DOI
29 Zhang Y, Mian MR, Chekhovskiy K, So S, Kupfer D, Lai H, Roe BA. Differential gene expression in Festuca under heat stress conditions. J Exp Bot 2005;56(413):897-907.   DOI
30 Mayer M, Bukau B. Hsp70 chaperones: cellular functions and molecular mechanism. Cell Mol Life Sci 2005;62(6):670.   DOI
31 Snoeck V, Peters IR, Cox E. The IgA system: a comparison of structure and function in different species. Vet Res 2006;37(3):455-67.   DOI
32 Racine R, McLaughlin M, Jones DD, Wittmer ST, MacNamara KC, Woodland DL, Winslow GM. IgM production by bone marrow plasmablasts contributes to long-term protection against intracellular bacterial infection. J Immunol 2011;186(2):1011-21.   DOI