Neuroprotective mechanism of sodium valproate and its application

doi:10.3969/j.issn.1006-7795.2017.03.008

Abstract

Abstract: As an inhibitor of histone deacetylases,sodium valproate is often used in the treatment of neuropsychiatric disorders such as antiepileptic treatment,schizophrenia and bipolar disorder. Sodium valproate can also affect the growth,mutation and apoptosis of neurons and play a neuroprotective effect. The mechanism of neuroprotection of sodium valproate is related to the regulation of neurotransmission and intracellular signaling pathways. Sodium valproate as a neuroprotective drug for the treatment of nerve injury and cognitive impairment remains to be further studied.

Key words: sodium valproate, neuroprotection, signal transduction, histone deacetylase inhibitor

CLC Number:

R971⁺.6

Liu Quanle, Li Tianfu, Wang Baoguo. Neuroprotective mechanism of sodium valproate and its application[J]. Journal of Capital Medical University, 2017, 38(3): 365-371.

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URL: https://journal03.magtech.org.cn/Jweb_sdykdxxb/EN/10.3969/j.issn.1006-7795.2017.03.008

https://journal03.magtech.org.cn/Jweb_sdykdxxb/EN/Y2017/V38/I3/365

References

[1] L scher W. Basic pharmacology of valproate:a review after 35 years of clinical use for the treatment of epilepsy[J]. CNS Drugs, 2002,16(10):669-694.
[2] Chen S, Wu H, Klebe D, et al. Valproic acid:a new candidate of therapeutic application for the acute central nervous system injuries[J]. Neurochem Res, 2014,39(9):1621-1633.
[3] Venkataraman V, Wheless J W. Safety of rapid intravenous infusion of valproate loading doses in epilepsy patients[J]. Epilepsy Res, 1999,35(2):147-153.
[4] Mattson R H, Cramer J A, Collins J F. A comparison of valproate with carbamazepine for the treatment of complex partial seizures and secondarily generalized tonic-clonic seizures in adults. The department of Veterans Affairs Epilepsy Cooperative Study No. 264 Group[J]. N Engl J Med, 1992,327(11):765-771.
[5] L scher W. Valproate:a reappraisal of its pharmacodynamic properties and mechanisms of action[J]. Prog Neurobiol, 1999,58(1):31-59.
[6] Hu J, Quick M W. Substrate-mediated regulation of gamma-aminobutyric acid transporter 1 in rat brain[J]. Neuropharmacology, 2008,54(2):309-318.
[7] Chiu C S, Brickley S, Jensen K, et al. GABA transporter deficiency causes tremor, ataxia, nervousness, and increased GABA-induced tonic conductance in cerebellum[J]. J Neurosci, 2005,25(12):3234-3245.
[8] Monti B, Polazzi E, Contestabile A. Biochemical, molecular and epigenetic mechanisms of valproic acid neuroprotection[J]. Curr Mol Pharmacol, 2009,2(1):93-109.
[9] Harrison N L, Simmonds M A. Sodium valproate enhances responses to GABA receptor activation only at high concentrations[J]. Brain Res, 1982,250(1):201-204.
[10] Motohashi N. GABA receptor alterations after chronic lithium administration. Comparison with carbamazepine and sodium valproate[J]. Prog Neuropsychopharmacol Biol Psychiatry, 1992,16(4):571-579.
[11] Cunningham M O, Woodhall G L, Jones R S. Valproate modifies spontaneous excitation and inhibition at cortical synapses in vitro[J]. Neuropharmacology, 2003,45(7):907-917.
[12] Thurston J H, Hauhart R E. Valproate doubles the anoxic survival time of normal developing mice:possible relevance to valproate-induced decreases in cerebral levels of glutamate and aspartate, and increases in taurine[J]. Life Sci, 1989,45(1):59-62.
[13] Hassel B, Iversen E G, Gjerstad L, et al. Up-regulation of hippocampal glutamate transport during chronic treatment with sodium valproate[J]. J Neurochem, 2001,77(5):1285-1292.
[14] VanDongen A M, VanErp M G, Voskuyl R A. Valproate reduces excitability by blockage of sodium and potassium conductance[J]. Epilepsia, 1986,27(3):177-182.
[15] Farber N B, Jiang X P, Heinkel C, et al. Antiepileptic drugs and agents that inhibit voltage-gated sodium channels prevent NMDA antagonist neurotoxicity[J]. Mol Psychiatry, 2002,7(7):726-733.
[16] G ttlicher M, Minucci S, Zhu P, et al. Valproic acid defines a novel class of HDAC inhibitors inducing differentiation of transformed cells[J]. EMBO J, 2001,20(24):6969-6978.
[17] Li Y, Alam H B. Modulation of acetylation:creating a pro-survival and anti-inflammatory phenotype in lethal hemorrhagic and septic shock[J]. J Biomed Biotechnol, 2011,2011:523481.
[18] Bambakidis T, Dekker S E, Liu B, et al. Hypothermia and valproic acid activate prosurvival pathways after hemorrhage[J]. J Surg Res, 2015,196(1):159-165.
[19] Brunet A, Datta S R, Greenberg M E. Transcription-dependent and -independent control of neuronal survival by the PI3K-Akt signaling pathway[J]. Curr Opin Neurobiol, 2001,11(3):297-305.
[20] Ren M, Leng Y, Jeong M, et al. Valproic acid reduces brain damage induced by transient focal cerebral ischemia in rats:potential roles of histone deacetylase inhibition and heat shock protein induction[J]. J Neurochem, 2004,89(6):1358-1367.
[21] Yuan P X, Huang L D, Jiang Y M, et al. The mood stabilizer valproic acid activates mitogen-activated protein kinases and promotes neurite growth[J]. J Biol Chem, 2001,276(34):31674-31683.
[22] Dekker S E, Bambakidis T, Sillesen M, et al. Effect of pharmacologic resuscitation on the brain gene expression profiles in a swine model of traumatic brain injury and hemorrhage[J]. J Trauma Acute Care Surg, 2014,77(6):906-912; discussion 912.
[23] Lucas S M, Rothwell N J, Gibson R M. The role of inflammation in CNS injury and disease[J]. Br J Pharmacol, 2006,147 Suppl 1:S232-240.
[24] Ahmad M, Graham S H. Inflammation after stroke:mechanisms and therapeutic approaches[J]. Transl Stroke Res, 2010,1(2):74-84.
[25] Chen P S, Wang C C, Bortner C D, et al. Valproic acid and other histone deacetylase inhibitors induce microglial apoptosis and attenuate lipopolysaccharide-induced dopaminergic neurotoxicity[J]. Neuroscience, 2007,149(1):203-212.
[26] Gibbons H M, Smith A M, Teoh H H, et al. Valproic acid induces microglial dysfunction, not apoptosis, in human glial cultures[J]. Neurobiol Dis, 2011,41(1):96-103.
[27] Zhang Z, Zhang Z Y, Wu Y, et al. Valproic acid ameliorates inflammation in experimental autoimmune encephalomyelitis rats[J]. Neuroscience, 2012,221:140-150.
[28] Bauernfeind F G, Horvath G, Stutz A, et al. Cutting edge:NF-kappaB activating pattern recognition and cytokine receptors license NLRP3 inflammasome activation by regulating NLRP3 expression[J]. J Immunol, 2009,183(2):787-791.
[29] Harder J, Franchi L, Muñoz-Planillo R, et al. Activation of the Nlrp3 inflammasome by Streptococcus pyogenes requires streptolysin O and NF-kappa B activation but proceeds independently of TLR signaling and P2X7 receptor[J]. J Immunol, 2009,183(9):5823-5829.
[30] Segovia J, Sabbah A, Mgbemena V, et al. TLR2/MyD88/NF-κB pathway, reactive oxygen species, potassium efflux activates NLRP3/ASC inflammasome during respiratory syncytial virus infection[J].PLoS One,2012,7(1):e29695.
[31] Latz E, Xiao T S, Stutz A. Activation and regulation of the inflammasomes[J]. Nat Rev Immunol, 2013,13(6):397-411.
[32] Kwon K J, Kim J N, Kim M K, et al. Neuroprotective effects of valproic acid against hemin toxicity:possible involvement of the down-regulation of heme oxygenase-1 by regulating ubiquitin-proteasomal pathway[J]. Neurochem Int, 2013,62(3):240-250.
[33] Wang Z, Leng Y, Tsai L K, et al. Valproic acid attenuates blood-brain barrier disruption in a rat model of transient focal cerebral ischemia:the roles of HDAC and MMP-9 inhibition[J]. J Cereb Blood Flow Metab, 2011,31(1):52-57.
[34] Wu X, Chen P S, Dallas S, et al. Histone deacetylase inhibitors up-regulate astrocyte GDNF and BDNF gene transcription and protect dopaminergic neurons[J]. Int J Neuropsychopharmacol, 2008,11(8):1123-1134.
[35] Bredy T W, Wu H, Crego C, et al. Histone modifications around individual BDNF gene promoters in prefrontal cortex are associated with extinction of conditioned fear[J]. Learn Mem, 2007,14(4):268-276.
[36] Yasuda S, Liang M H, Marinova Z, et al. The mood stabilizers lithium and valproate selectively activate the promoter IV of brain-derived neurotrophic factor in neurons[J]. Mol Psychiatry, 2009,14(1):51-59.
[37] Cui J, Shao L, Young L T, et al. Role of glutathione in neuroprotective effects of mood stabilizing drugs lithium and valproate[J]. Neuroscience, 2007,144(4):1447-1453.
[38] Shao L, Young L T, Wang J F. Chronic treatment with mood stabilizers lithium and valproate prevents excitotoxicity by inhibiting oxidative stress in rat cerebral cortical cells[J]. Biol Psychiatry, 2005,58(11):879-884.
[39] Li Y, Yuan Z, Liu B, et al. Prevention of hypoxia-induced neuronal apoptosis through histone deacetylase inhibition[J]. J Trauma, 2008,64(4):863-870. discussion 870-871.
[40] Bramlett H M, Dietrich W D. Progressive damage after brain and spinal cord injury:pathomechanisms and treatment strategies[J]. Prog Brain Res, 2007,161:125-141.
[41] Kadhim H J, Duchateau J, Sébire G. Cytokines and brain injury:invited review[J]. J Intensive Care Med, 2008,23(4):236-249.
[42] Faden A I, Demediuk P, Panter S S, et al. The role of excitatory amino acids and NMDA receptors in traumatic brain injury[J]. Science, 1989,244(4906):798-800.
[43] Zhang X, Chen Y, Jenkins L W, et al. Bench-to-bedside review:Apoptosis/programmed cell death triggered by traumatic brain injury[J]. Crit Care, 2005,9(1):66-75.
[44] Raghupathi R. Cell death mechanisms following traumatic brain injury[J]. Brain Pathol, 2004,14(2):215-222.
[45] Dash P K, Orsi S A, Zhang M, et al. Valproate administered after traumatic brain injury provides neuroprotection and improves cognitive function in rats[J]. PLoS One, 2010,5(6):e11383.
[46] Sinn D I, Kim S J, Chu K, et al. Valproic acid-mediated neuroprotection in intracerebral hemorrhage via histone deacetylase inhibition and transcriptional activation[J]. Neurobiol Dis, 2007,26(2):464-472.
[47] Meaney D F, Ross D T, Winkelstein B A, et al. Modification of the cortical impact model to produce axonal injury in the rat cerebral cortex[J]. J Neurotrauma, 1994,11(5):599-612.
[48] Biermann J, Grieshaber P, Goebel U, et al. Valproic acid-mediated neuroprotection and regeneration in injured retinal ganglion cells[J]. Invest Ophthalmol Vis Sci, 2010,51(1):526-534.
[49] Bredy T W, Wu H, Crego C, et al. Histone modifications around individual BDNF gene promoters in prefrontal cortex are associated with extinction of conditioned fear[J]. Learn Mem, 2007,14(4):268-276.