CJRTP

Chinese Journal of Rehabilitation Theory and Practice >

2020 , Vol. 26 >Issue 3: 330 - 333

DOI: https://doi.org/10.3969/j.issn.1006-9771.2020.03.013

Role of Kelch-like ECH-associated Protein-1-Nuclear Factor Erythroid 2-related Factor-2/Antioxidant Responsive Element Signal Pathway for Multiple Sclerosis (review)

  • Ling-ling SU ,
  • Bi-e ZHENG ,
  • Jin-di HE ,
  • Jian-zhong FAN ,
  • Rui-xue YIN
Expand
  • Department of Rehabilitation Medicine, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong 510515, China

Received date: 2018-12-20

  Revised date: 2019-01-29

  Online published: 2020-04-01

Supported by

Guangdong Natural Science Foundation(2016A030313523)

Fold

Abstract

Multiple sclerosis (MS) is a chronic inflammatory disease, mainly due to the activation of the T cells, which makes oxidative stress reaction in brain and leads to demyelination finally. Kelch-like ECH-associated protein-1 (Keap1)-nuclear factor erythroid 2-related factor-2 (Nrf2)/antioxidant responsive element (ARE) signal pathway is one of the most important endogenous antioxidant pathways, which promotes the expression of detoxification enzymes and antioxidant protein to eliminate oxygen free radicals and balance intracellular redox system. Activation of the Keap1-Nrf2/ARE may delay the progression of MS by drugs or rehabilitation.

Key words： multiple sclerosis; oxidative stress; Kelch-like ECH-associated protein-1; nuclear factor E2-related factor-2; antioxidant responsive element; signal pathway; review

Cite this article

Ling-ling SU , Bi-e ZHENG , Jin-di HE , Jian-zhong FAN , Rui-xue YIN . Role of Kelch-like ECH-associated Protein-1-Nuclear Factor Erythroid 2-related Factor-2/Antioxidant Responsive Element Signal Pathway for Multiple Sclerosis (review)[J]. Chinese Journal of Rehabilitation Theory and Practice, 2020 , 26(3) : 330 -333 . DOI: 10.3969/j.issn.1006-9771.2020.03.013

References

[1] Sánchez-López A L, Ortiz G G, Pacheco-Moises F P, et al. Efficacy of melatonin on serum pro-inflammatory cytokines and oxidative stress markers in relapsing remitting multiple sclerosis[J]. Arch Med Res, 2018, 49(6):391-398.
[2] Glass C K, Saijo K, Winner B, et al. Mechanisms underlying inflammation in neurodegeneration[J]. Cell, 2010, 140(6):918-934.
[3] Harrison K. Fingolimod for multiple sclerosis: a review for the specialist nurse[J]. Br J Nurs, 2014, 23(11):582-589.
[4] Ohl K, Tenbrock K, Kipp M. Oxidative stress in multiple sclerosis: central and peripheral mode of action[J]. Exp Neurol, 2016, 277:58-67.
[5] Compston A, Coles A. Multiple sclerosis[J]. Lancet, 2008, 372(9648):1502-1517.
[6] Lim J L, Wilhelmus M M, de Vries H E, et al. Antioxidative defense mechanisms controlled by Nrf2: state-of-the-art and clinical perspectives in neurodegenerative diseases[J]. Arch Toxicol, 2014, 88(10):1773-1786.
[7] Feinstein A, Freeman J, Lo A C. Treatment of progressive multiple sclerosis: what works, what does not, and what is needed[J]. Lancet Neurol, 2015, 14(2):194-207.
[8] Chaudhuri A. Multiple sclerosis is primarily a neurodegenerative disease[J]. J Neural Transm (Vienna), 2013, 120(10):1463-1466.
[9] Liddell J R. Are astrocytes the predominant cell type for activation of Nrf2 in aging and neurodegeneration?[J]. Antioxidants (Basel), 2017, 6(3):E65.
[10] Islam M T. Oxidative stress and mitochondrial dysfunction-linked neurodegenerative disorders[J]. Neurol Res, 2017, 39(1):73-82.
[11] Haider L, Fischer M T, Frischer J M, et al. Oxidative damage in multiple sclerosis lesions[J]. Brain, 2011, 134(Pt 7):1914-1924.
[12] Lim J L, Wilhelmus M M M, de Vries H E, et al. Antioxidative defense mechanisms controlled by Nrf2: state-of-the-art and clinical perspectives in neurodegenerative diseases[J]. Arch Toxicol, 2014, 88(10):1773-1786.
[13] Mahad D, Ziabreva I, Lassmann H, et al. Mitochondrial defects in acute multiple sclerosis lesions[J]. Brain, 2008, 131(Pt 7):1722-1735.
[14] Campbell G R, Ziabreva I, Reeve A K, et al. Mitochondrial DNA deletions and neurodegeneration in multiple sclerosis[J]. Ann Neurol, 2011, 69(3):481-492.
[15] van Horssen J, Schreibelt G, Drexhage J, et al. Severe oxidative damage in multiple sclerosis lesions coincides with enhanced antioxidant enzyme expression[J]. Free Radic Biol Med, 2008, 45(12):1729-1737.
[16] Buendia I, Michalska P, Navarro E, et al. Nrf2-ARE pathway: An emerging target against oxidative stress and neuroinflammation in neurodegenerative diseases[J]. Pharmacol Ther, 2016, 157:84-104.
[17] Ren H L, Lv C N, Xing Y, et al. Downregulated nuclear factor E2-related factor 2 (Nrf2) aggravates cognitive impairments via neuroinflammation and synaptic plasticity in the senescence-accelerated mouse prone 8 (SAMP8) mouse: a model of accelerated senescence[J]. Med Sci Monit, 2018, 24:1132-1144.
[18] Kim J, Cha Y N, Surh Y J. A protective role of nuclear factor-erythroid 2-related factor-2 (Nrf2) in inflammatory disorders[J]. Mutat Res, 2010, 690(1-2):12-23.
[19] Gazaryan I G, Thomas B. The status of Nrf2-based therapeutics: current perspectives and future prospects[J]. Neural Regen Res, 2016, 11(11):1708-1711.
[20] Niture S K, Khatri R, Jaiswal A K. Regulation of Nrf2–an update[J]. Free Radic Biol Med, 2014, 66:36-44.
[21] Canning P, Sorrell F J, Bullock A N. Structural basis of Keap1 interactions with Nrf2[J]. Free Radic Biol Med, 2015, 88(Pt B):101-107.
[22] Suzuki T, Yamamoto M. Molecular basis of the Keap1-Nrf2 system[J]. Free Radic Biol Med, 2015, 88(Pt B):93-100.
[23] Hu R, Saw C L, Yu R, et al. Regulation of NF-E2-related factor 2 signaling for cancer chemoprevention: antioxidant coupled with antiinflammatory[J]. Antioxid Redox Signal, 2010, 13(11):1679-1698.
[24] Keum Y S. Regulation of Nrf2-mediated phase II detoxification and anti-oxidant genes[J]. Biomol Ther (Seoul), 2012, 20(2):144-151.
[25] Cullinan S B, Diehl J A. PERK-dependent activation of Nrf2 contributes to redox homeostasis and cell survival following endoplasmic reticulum stress[J]. J Biol Chem, 2004, 279(19):20108-20117.
[26] Lu M C, Ji J A, Jiang Z Y, et al. The Keap1-Nrf2-ARE pathway as a potential preventive and therapeutic target: an update[J]. Med Res Rev, 2016, 36(5):924-963.
[27] Karkkainen V, Pomeshchik Y, Savchenko E, et al. Nrf2 regulates neurogenesis and protects neural progenitor cells against Abeta toxicity[J]. Stem Cells, 2014, 32(7):1904-1916.
[28] van Muiswinkel F L, de Vos R A, Bol J G, et al. Expression of NAD(P)H: quinone oxidoreductase in the normal and Parkinsonian substantia nigra[J]. Neurobiol Aging, 2004, 25(9):1253-1262.
[29] Gao Y, Chu S F, Li J P, et al. Protopanaxtriol protects against 3-nitropropionic acid-induced oxidative stress in a rat model of Huntington's disease[J]. Acta Pharmacol Sin, 2015, 36(3):311-322.
[30] Chen M J Wong C H Y Peng Z F, et al. A global transcriptomic view of the multifaceted role of glutathione peroxidase-1 in cerebral ischemic-reperfusion injury[J]. Free Radic Biol Med, 2011, 50(6):736-748.
[31] Lisk C, Mccord J, Bose S, et al. Nrf2 activation: a potential strategy for the prevention of acute mountain sickness[J]. Free Radic Biol Med, 2013, 63:264-273.
[32] Kundu J K, Surh Y J. Nrf2-Keap1 signaling as a potential target for chemoprevention of inflammation-associated carcinogenesis[J]. Pharm Res, 2010, 27(6):999-1013.
[33] van Horssen J, Schreibelt G, Bo L, et al. NAD(P)H: quinone oxidoreductase 1 expression in multiple sclerosis lesions[J]. Free Radic Biol Med, 2006, 41(2):311-317.
[34] Ryter S W, Choi A M. Heme oxygenase-1/carbon monoxide: from metabolism to molecular therapy[J]. Am J Respir Cell Mol Biol, 2009, 41(3):251-260.
[35] Licht-Mayer S, Wimmer I, Traffehn S, et al. Cell type-specific Nrf2 expression in multiple sclerosis lesions[J]. Acta Neuropathologica, 2015, 130(2):263-277.
[36] Dringen R. Metabolism and functions of glutathione in brain[J]. Prog Neurobiol, 2000, 62(6):649-671.
[37] Johnson D A, Amirahmadi S, Ward C, et al. The absence of the pro-antioxidant transcription factor Nrf2 exacerbates experimental autoimmune encephalomyelitis[J]. Toxicol Sci, 2010, 114(2):237-246.
[38] Bernstein A I, Miller G W. Oxidative signaling in experimental autoimmune encephalomyelitis[J]. Toxicol Sci, 2010, 114(2):159-161.
[39] Linker R A, Lee D, Ryan S, et al. Fumaric acid esters exert neuroprotective effects in neuroinflammation via activation of the Nrf2 antioxidant pathway[J]. Brain, 2011, 134(3):678-692.
[40] Scannevin R H, Chollate S, Jung M Y, et al. Fumarates promote cytoprotection of central nervous system cells against oxidative stress via the nuclear factor (erythroid-derived 2)-like 2 pathway[J]. J Pharmacol Exp Ther, 2012, 341(1):274-284.
[41] Tutakhail A, Nazary Q A, Lebsir D, et al. Induction of brain Nrf2-HO-1 pathway and antinociception after different physical training paradigms in mice[J]. Life Sci, 2018, 209:149-156.
[42] Babayi Daylari T, Riazi G H, Pooyan S, et al. Influence of various intensities of 528 Hz sound-wave in production of testosterone in rat’s brain and analysis of behavioral changes[J]. Genes Genomics, 2019, 41(2):201-211.
[43] 杜韬, 张威. 眼针八区八穴对急性脑梗死Keap1-Nrf2/ARE信号传导通路的影响[J]. 中华中医药学刊, 2018, 36(8):1837-1840.
[44] Boyanapalli S S, Paredes-Gonzalez X, Fuentes F, et al. Nrf2 knockout attenuates the anti-inflammatory effects of phenethyl isothiocyanate and curcumin[J]. Chem Res Toxicol, 2014, 27(12):2036-2043.
[45] Holloway P M, Gillespie S, Becker F, et al. Sulforaphane induces neurovascular protection against a systemic inflammatory challenge via both Nrf2-dependent and independent pathways[J]. Vascul Pharmacol, 2016, 85:29-38.
[46] Turley A E, Zagorski J W, Rockwell C E. The Nrf2 activator tBHQ inhibits T cell activation of primary human CD4 T cells[J]. Cytokine, 2015, 71(2):289-295.
[47] Souza P S, Gonçalves E D, Pedroso G S, et al. Physical exercise attenuates experimental autoimmune encephalomyelitis by inhibiting peripheral immune response and blood-brain barrier disruption[J]. Mol Neurobiol, 2017, 54(6):4723-4737.
Options
Outlines

/

〈 〉