BMC Complementary and Alternative Medicine | |
Mechanistic basis for protection of differentiated SH-SY5Y cells by oryzanol-rich fraction against hydrogen peroxide-induced neurotoxicity | |
Muhammad Firdaus Abu Bakar2  Jhi Biau Foo2  Siti Farhana Fathy2  Nur Hanisah Azmi2  Mustapha Umar Imam2  Maznah Ismail1  Norsharina Ismail2  | |
[1] Department of Nutrition and Dietetics, Faculty of Medicine and Health Sciences, Universiti Putra Malaysia, Serdang, Selangor 43400, Malaysia;Nutricosmeceuticals and Nutrigenomics Programme, Laboratory of Molecular Biomedicine, Institute of Bioscience, Universiti Putra Malaysia, Serdang, Selangor 43400, Malaysia | |
关键词: SH-SY5Y cells; Multiplex GeXP; Supercritical fluid extraction system; Hydrogen peroxide; Oryzanol-rich fraction; Rice bran; Neuroprotective; | |
Others : 1229020 DOI : 10.1186/1472-6882-14-467 |
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received in 2014-04-22, accepted in 2014-11-21, 发布年份 2014 | |
【 摘 要 】
Background
Apoptosis is often the end result of oxidative damage to neurons. Due to shared pathways between oxidative stress, apoptosis and antioxidant defence systems, an oxidative insult could end up causing cellular apoptosis or survival depending on the severity of the insult and cellular responses. Plant bioresources have received close attention in recent years for their potential role in regulating the pathways involved in apoptosis and oxidative stress in favour of cell survival. Rice bran is a bioactive-rich by-product of rice milling process. It possesses antioxidant properties, making it a promising source of antioxidants that could potentially prevent oxidative stress-induced neurodegenerative diseases.
Methods
Thus, the present study investigated the neuroprotective properties of oryzanol-rich fraction (ORF) against hydrogen peroxide (H2O2)-induced neurotoxicity in differentiated human neuroblastoma SH-SY5Y cells. ORF was extracted from rice bran using a green technology platform, supercritical fluid extraction system. Furthermore, its effects on cell viability, morphological changes, cell cycle, and apoptosis were evaluated. The underlying transcriptomic changes involved in regulation of oxidative stress, apoptosis and antioxidant defence systems were equally studied.
Results
ORF protected differentiated SH-SY5Y cells against H2O2-induced neurotoxicity through preserving the mitochondrial metabolic enzyme activities, thus reducing apoptosis. The mechanistic basis for the neuroprotective effects of ORF included upregulation of antioxidant genes (catalase, SOD 1 and SOD 2), downregulation of pro-apoptotic genes (JNK, TNF, ING3, BAK1, BAX, p21 and caspase-9), and upregulation of anti-apoptotic genes (ERK1/2, AKT1 and NF-Kβ).
Conclusion
These findings suggest ORF may be an effective antioxidant that could prevent oxidative stress-induced neurodegenerative disorders.
【 授权许可】
2014 Ismail et al.; licensee BioMed Central.
【 预 览 】
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【 参考文献 】
- [1]Martindale JL, Holbrook NJ: Cellular response to oxidative stress: signaling for suicide and survival. J Cell Physiol 2002, 192(1):1-15.
- [2]Melo A, Monteiro L, Lima RMF, De Oliveira DM, De Cerqueira MD, El-Bachá RS: Oxidative stress in neurodegenerative diseases: mechanisms and therapeutic perspectives. Oxid Med Cell Longev 2011, 2011:467180.
- [3]Sugawara T, Fujimura M, Noshita N, Kim GW, Saito A, Hayashi T, Narasimhan P, Maier CM, Chan PH: Neuronal death/survival signaling pathways in cerebral ischemia. Neuro RX 2004, 1(1):17-25.
- [4]Mattson MP, Camandola S: NF-κB in neuronal plasticity and neurodegenerative disorders. J Clin Invest 2001, 107(3):247-254.
- [5]Laokuldilok T, Shoemaker CF, Jongkaewwattana S, Tulyathan V: Antioxidants and antioxidant activity of several pigmented rice brans. J Agric Food Chem 2011, 59:193-199.
- [6]Jariwalla RJ: Rice-bran products: phytonutrients with potential applications in preventive and clinical medicine. Drugs ExpClin Res 2001, 27:17-26.
- [7]Ha TY, Han S, Kim SR, Kim IH, Lee HY, Kim HK: Bioactive components in rice bran oil improve lipid profiles in rats fed a high-cholesterol diet. Nutr Res 2005, 25:597-606.
- [8]Jeng TL, Ho PT, Shih YJ, Lai CC, Wu MT, Sung JM: Comparisons of protein, lipid, phenolics, γ-oryzanol, vitamin E, and mineral contents in bran layer of sodium azide-induced red rice mutants. J Sci Food Agric 2011, 91:1459-1465.
- [9]Fabian C, Ju YH: A review on rice bran protein: its properties and extraction methods. Crit Rev Food Sci Nutr 2011, 51:816-827.
- [10]Ermak S, Dunford NT: Policosanol contents and composition of wheat varieties. J Agric Food Chem 2005, 53:5583-5586.
- [11]Wang T, Hicks KB, Moreau R: Antioxidant activity of phytosterols, oryzanol, and other phytosterols conjugates. J Am Oil Chem Soc 2002, 79:1201-1206.
- [12]Srinivasan M, Sudheer AR, Menon VP: Ferulic acid: therapeutic potential through its antioxidant property. J Clin Biochem Nutr 2007, 40:92-100.
- [13]Hudson EA, Dinh PA, Kokubun T, Simmonds MS, Gescher A: Characterization of potentially chemopreventive phenols in extracts of brown rice that inhibit the growth of human breast and colon cancer cells. Cancer Epidemiol Biomarkers Prev 2000, 9(11):1163-1170.
- [14]Ardiansyah SH, Koseki T, Hashizume K, Komai M: The Driselase-treated fraction of rice bran is a more effective dietary factor to improve hypertension, glucose and lipid metabolism in stroke-prone spontaneously hypertensive rats compared to ferulic acid. Br J Nutr 2007, 97:67-76.
- [15]Kaup RM, Khayyal MT, Verspohl EJ: Antidiabetic effects of standardized Egyptian rice bran extract. Phytother Res 2013, 27(2):264-271.
- [16]Al-Naqeep G, Ismail M, Allaudin Z: Regulation of low-density lipoprotein receptor and 3-hydroxy-3-methylglutaryl coenzyme A reductase gene expression by thymoquinone-rich fraction and thymoquinone in HepG2 cells. J Nutrigenet Nutrigenomics 2009, 2:163-172.
- [17]Chan KW, Ismail M: Supercritical carbon dioxide fluid extraction of Hibiscus cannabinus L. seed oil: a potential solvent-free and high antioxidative edible oil. Food Chem 2009, 114:970-975.
- [18]Ismail M, Al-Naqeeb G, Mamat WA, Ahmad Z: Gamma-oryzanol rich fraction regulates the expression of antioxidant and oxidative stress related genes in stressed rat’s liver. Nutr Met 2010, 7(23):1-13.
- [19]Ismail M, Al-Naqeep G, Chan KW: Nigella sativa thymoquinone-rich fraction greatly improves plasma antioxidant capacity and expression of antioxidant genes in hypercholesterolemic rats. Free Radic Biol Med 2010, 48:664-672.
- [20]Norsharina I, Maznah I, Aied A, Al-Naqeeb G: Thymoquinone rich fraction from Nigella sativa and thymoquinone are cytotoxic towards colon and leukemic carcinoma cell lines. J Med Plants Res 2011, 5(15):3359-3366.
- [21]Mariod AA, Mattha¨us B, Ismail M: Comparison of supercritical fluid and hexane extraction methods in extracting Kenaf (Hibiscus cannabinus) seed oil lipids. J Am Oil Chem Soc 2011, 88:931-935.
- [22]Foo JB, Yazan LS, Mansor SM, Ismail N, Tahir PM, Ismail M: Kenaf seed oil from supercritical carbon dioxide fluid extraction inhibits the proliferation of WEHI-3B leukemia cells in vivo. J Med Plants Res 2012, 6(8):1429-1436.
- [23]Ghafar SAA, Ismail M, Yazan LS, Fakurazi S, Ismail N, Chan KW, Tahir PM: Cytotoxic activity of Kenaf seed oils from supercritical carbon dioxide fluid extraction towards human colorectal cancer (HT29) cell lines. Evid Based Complement Alternat Med 2013, 2013:549705.
- [24]Ismail N, Ismail M, Fathy SF, Musa SNA, Imam MU, Foo JB, Iqbal S: Neuroprotective effects of germinated brown rice against hydrogen peroxide induced cell death in human SH-SY5Y cells. Int J Mol Sci 2012, 13:9692-9708.
- [25]Klein JA, Ackerman SL: Oxidative stress, cell cycle, and neurodegeneration. J Clin Invest 2003, 111(6):785-793.
- [26]Gandhi S, Abramov AY: Mechanism of oxidative stress in neurodegeneration. Oxid Med Cell Longev 2012, 2012:428010.
- [27]Pocernich CB, Lange ML, Sultana R, Butterfield DA: Nutritional approaches to modulate oxidative stress in Alzheimer’s disease. Curr Alzheimer Res 2011, 8(5):452-469.
- [28]Azmi NH, Ismail N, Imam MU, Ismail M: Ethyl acetate extract of germinated brown rice attenuates hydrogen peroxide-induced oxidative stress in human SH-SY5Y neuroblastoma cells: role of anti-apoptotic, pro-survival and antioxidant genes. BMC Complement Alternat Med 2013, 13:177. BioMed Central Full Text
- [29]Liu CL, Xie LX, Li M, Durairajan SSK, Goto S, Huang JD: Salvianolic acid B inhibits hydrogen peroxide-induced endothelial cell apoptosis through regulating PI3K/Akt signalling. PLoS One 2007, 12:e1321.
- [30]Pugazhenthi S, Wang M, Pham S, Sze CI, Eckman CB: Downregulation of CREB expression in Alzheimer’s brain and in Aβ-treated rat hippocampal neurons. Mol Neurodegener 2011, 6:60. BioMed Central Full Text
- [31]Yi-Rong C, Anju S, Tse-Hua T: Down-regulation of the c-Jun N-terminal kinase (JNK) phosphatase M3/6 and activation of JNK by hydrogen peroxide and pyrrolidinedithiocarbamate. Oncogene Res 2001, 20:367-374.
- [32]Kutuk O, Basaga H: Apoptosis signalling by 4-hydroxynonenal: a role for JNK-c-Jun/AP-1 pathway. Redox Rep 2007, 12(1):30-34.
- [33]Luo J, Robinson JP, Shi R: Acrolein-induced cell death in PC12 cells: role of mitochondria-mediated oxidative stress. Neurochem Int 2005, 47:449-457.
- [34]Sachsenmaier C, Radler-Pohl A, Zinck R, Nordheim A, Herrlich P, Rahmsdorf HJ: Involvement of growth factor receptors in the mammalian UVC response. Cell 1994, 78:963-972.
- [35]Schieven GL, Mittler RS, Nadler SG, Kirihara JM, Bolen JB, Kanner SB, Ledbetter JA: ZAP-70 tyrosine kinase, CD45, and T cell receptor involvement in UV- and H2O2-induced T cell signal transduction. J Biol Chem 1994, 269:20718-20726.
- [36]Huang RP, Wu JX, Fan Y, Adamson ED: UV activates growth factor receptors via reactive oxygen intermediates. J Cell Biol 1996, 133:211-220.
- [37]Guyton KZ, Gorospe M, Wang X, Mock YD, Kokkonen GC, Liu Y, Roth GS, Holbrook NJ: Age-related changes in activation of mitogen-activated protein kinase cascades by oxidative stress. J Investig Dermatol Symp Proc 1998, 3:23-27.
- [38]Guyton KZ, Gorospe M, Kensler TW, Holbrook NJ: Mitogen activated protein kinase (MAPK) activation by butylatedhydroxytoluenehydroperoxide: implications for cellular survival and tumor promotion. Cancer Res 1996, 56:3480-3485.
- [39]Guyton KZ, Liu Y, Gorospe M, Xu Q, Holbrook NJ: Activation of mitogen-activated protein kinase by H2O2. Role in cell survival following oxidant injury. J Biol Chem 1996, 271:4138-4142.
- [40]Thornton TM, Rincon M: Non-classical p38 Map Kinase functions: cell cycle checkpoints and survival. Int J BiolSci 2009, 5(1):44-52.
- [41]Wang X, McCullough KD, Franke TF, Holbrook NJ: Epidermal growth factor receptor-dependent Akt activation by oxidative stress enhances cell survival. J Biol Chem 2000, 275:14624-14631.
- [42]Canas N, Valero T, Villarroya M, Montell E, Vergés J, García AG, López MG: Chondroitin sulfate protects SH-SY5Y cells from oxidative stress by inducing heme oxygenase-1 via phosphatidylinositol 3-kinase/Akt. J Pharmacol Exp Ther 2007, 323:946-953.
- [43]Heo SR, Han AM, Kwon YK, Joung I: p62 protects SH-SY5Y neuroblastoma cells against H2O2-induced injury through the PDK1/Akt pathway. Neurosci Lett 2009, 450:45-50.
- [44]Nagashima M, Shiseki M, Pedeux RM, Okamura S, Kitahama-Shiseki M, Miura K, Yokota J, Harris CC: A novel PHD-finger motif protein, p47ING3, modulates p53-mediated transcription, cell cycle control, and apoptosis. Oncogene 2003, 22:343-350.