Progress of mechanism of oxidative stress in acute ischemic stroke

doi:10.3877/cma.j.issn.2095-9141.2021.02.013

Abstract

Abstract:

Stroke is the leading cause of death in China, while oxidative stress persists throughout the disease. Antioxidative is an important treatment method to prevent nerve injury and promote the recovery of neurological function after ischemic stroke. However, its clinical application effect is still not satisfactory. This article reviews the research progress of oxidative stress related mechanisms in ischemic stroke in recent years, which support finding better transformation ideas, and at last promote the study of treatment of acute ischemic stroke.

Key words: Acute ischemic stroke, Cerebral infarction, Reactive oxygen species, Oxidative stress

Yiming Du, Xin Chen, Shiguang Zhao. Progress of mechanism of oxidative stress in acute ischemic stroke[J]. Chinese Journal of Neurotraumatic Surgery(Electronic Edition), 2021, 07(02): 121-124.

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References 43

[1]	Maciejczyk M, Żebrowska E, Chabowski A. Insulin resistance and oxidative stress in the brain: what’s new?[J]. Int J Mol Sci, 2019, 20(4): 874.
[2]	Zhang K, Tu M, Gao W, et al. Hollow prussian blue nanozymes drive neuroprotection against ischemic stroke via attenuating oxidative stress, counteracting inflammation, and suppressing cell apoptosis[J]. Nano Lett, 2019, 19(5): 2812-2823.
[3]	Brand MD. Mitochondrial generation of superoxide and hydrogen peroxide as the source of mitochondrial redox signaling[J]. Free Radic Biol Med, 2016, 100: 14-31.
[4]	Hanafy KA, Gomes JA, Selim M. Rationale and current evidence for testing iron chelators for treating stroke[J]. Curr Cardiol Rep, 2019, 21(4): 20.
[5]	Burmistrova O, Olias-Arjona A, Lapresa R, et al. Targeting PFKFB3 alleviates cerebral ischemia-reperfusion injury in mice[J]. Sci Rep, 2019, 9(1): 11670.
[6]	Amantea D, Bagetta G. Excitatory and inhibitory amino acid neurotransmitters in stroke: from neurotoxicity to ischemic tolerance[J]. Curr Opin Pharmacol, 2017, 35: 111-119.
[7]	Shi M, Cao L, Cao X, et al. DR-region of Na+/K+ ATPase is a target to treat excitotoxicity and stroke[J]. Cell Death Dis, 2018, 10(1): 6.
[8]	Chuang DY, Simonyi A, Kotzbauer PT, et al. Cytosolic phospholipase A2 plays a crucial role in ROS/NO signaling during microglial activation through the lipoxygenase pathway[J]. J Neuroinflammation, 2015, 12: 199.
[9]	Chouchani ET, Pell VR, Gaude E, et al. Ischaemic accumulation of succinate controls reperfusion injury through mitochondrial ROS[J]. Nature, 2014, 515(7527): 431-435.
[10]	Velimirović M, Jevtić Dožudić G, Selaković V, et al. Effects of vitamin D3 on the NADPH oxidase and matrix metalloproteinase 9 in an animal model of global cerebral ischemia[J]. Oxid Med Cell Longev, 2018, 2018: 3273654.
[11]	Chuang DY, Cui J, Simonyi A, et al. Dietary Sutherlandia and elderberry mitigate cerebral ischemia-induced neuronal damage and attenuate p47phox and phospho-ERK1/2 expression in microglial cells[J]. ASN Neuro, 2014, 6(6): 1759091414554946.
[12]	Liu Y, Feng S, Subedi K, et al. Attenuation of ischemic stroke-caused brain injury by a monoamine oxidase inhibitor involves improved proteostasis and reduced neuroinflammation[J]. Mol Neurobiol, 2020, 57(2): 937-948.
[13]	Kawai T, Okochi Y, Ozaki T, et al. Unconventional role of voltage-gated proton channels (VSOP/Hv1) in regulation of microglial ROS production[J]. J Neurochem, 2017, 142(5): 686-699.
[14]	Tang Z, Gan Y, Liu Q, et al. CX3CR1 deficiency suppresses activation and neurotoxicity of microglia/macrophage in experimental ischemic stroke[J]. J Neuroinflammation, 2014, 11: 26.
[15]	Nissanka N, Moraes CT. Mitochondrial DNA damage and reactive oxygen species in neurodegenerative disease[J]. FEBS Lett, 2018, 592(5): 728-742.
[16]	Jadavji NM, Farr TD, Lips J, et al. Elevated levels of plasma homocysteine, deficiencies in dietary folic acid and uracil-DNA glycosylase impair learning in a mouse model of vascular cognitive impairment[J]. Behav Brain Res, 2015, 283: 215-226.
[17]	Morris-Blanco KC, Kim T, Lopez MS, et al. Induction of DNA hydroxymethylation protects the brain after stroke[J]. Stroke, 2019, 50(9): 2513-2521.
[18]	Singh M, Kapoor A, Bhatnagar A. Oxidative and reductive metabolism of lipid-peroxidation derived carbonyls[J]. Chem Biol Interact, 2015, 234: 261-273.
[19]	Kotani S, Izawa S, Komai N, et al. Mitochondria-localized phospholipase A 2, AoPlaA, in aspergillus oryzae displays phosphatidylethanolamine-specific activity and is involved in the maintenance of mitochondrial phospholipid composition[J]. Fungal Genet Biol, 2016, 96: 1-11.
[20]	Stockwell BR, Friedmann Angeli JP, Bayir H, et al. Ferroptosis: a regulated cell death nexus linking metabolism, redox biology, and disease[J]. Cell, 2017, 171(2): 273-285.
[21]	Matsui R, Honda R, Kanome M, et al. Designing antioxidant peptides based on the antioxidant properties of the amino acid side-chains[J]. Food Chem, 2018, 245: 750-755.
[22]	Xu B, Qin Y, Li D, et al. Inhibition of PDE4 protects neurons against oxygen-glucose deprivation-induced endoplasmic reticulum stress through activation of the Nrf-2/HO-1 pathway[J]. Redox Biol, 2020, 28: 101342.
[23]	Xing J, Xu H, Liu C, et al. Melatonin ameliorates endoplasmic reticulum stress in N2a neuroblastoma cell hypoxia-reoxygenation injury by activating the AMPK-Pak2 pathway[J]. Cell Stress Chaperones, 2019, 24(3): 621-633.
[24]	Grochowski C, Litak J, Kamieniak P, et al. Oxidative stress in cerebral small vessel disease. Role of reactive species[J]. Free Radic Res, 2018, 52(1): 1-13.
[25]	Zhao M, Zhu P, Fujino M, et al. Oxidative stress in hypoxic-ischemic encephalopathy: molecular mechanisms and therapeutic strategies[J]. Int J Mol Sci, 2016, 17(12): 2078.
[26]	Jiang S, Deng C, Lv J, et al. Nrf2 weaves an elaborate network of neuroprotection against stroke[J]. Mol Neurobiol, 2017, 54: 1440-1455.
[27]	Tu LF, Cao LF, Zhang YH, et al. Sirt3-dependent deacetylation of COX-1 counteracts oxidative stress-induced cell apoptosis[J]. FASEB J, 2019, 33(12): 14118-14128.
[28]	Wei Y, Wang R, Teng J. Inhibition of calcium/calmodulin-dependent protein kinase IIalpha suppresses oxidative stress in cerebral ischemic rats through targeting glucose 6-phosphate dehydrogenase[J]. Neurochem Res, 2019, 44(7): 1613-1620.
[29]	Ye Y, Jin T, Zhang X, et al. Meisoindigo protects against focal cerebral ischemia-reperfusion injury by inhibiting NLRP3 inflammasome activation and regulating microglia/macrophage polarization via TLR4/NF-κB signaling pathway[J]. Front Cell Neurosci, 2019, 13: 553.
[30]	Bhat SA, Sood A, Shukla R, et al. AT2R Activation prevents microglia pro-inflammatory activation in a NOX-dependent manner: inhibition of PKC activation and p47phox phosphorylation by PP2A[J]. Mol Neurobiol, 2019, 56(4): 3005-3023.
[31]	Gonçalves LV, Herlinger AL, Ferreira TAA, et al. Environmental enrichment cognitive neuroprotection in an experimental model of cerebral ischemia: biochemical and molecular aspects[J]. Behav Brain Res, 2018, 348: 171-183.
[32]	Singhal G, Baune BT. Microglia: an interface between the loss of neuroplasticity and depression[J]. Front Cell Neurosci, 2017, 11: 270.
[33]	Jayaraj RL, Azimullah S, Beiram R, et al. Neuroinflammation: friend and foe for ischemic stroke[J]. J Neuroinflammation, 2019, 169(1): 142.
[34]	Liu Q, Zhang Y. PRDX1 enhances cerebral ischemia-reperfusion injury through activation of TLR4-regulated inflammation and apoptosis[J]. Biochem Biophys Res Commun, 2019, 519(3): 453-461.
[35]	Yang Q, Huang Q, Hu Z, et al. Potential neuroprotective treatment of stroke: targeting excitotoxicity, oxidative stress, and inflammation[J]. Front Neurosci, 2019, 13: 1036.
[36]	Yan W, Sun W, Fan J. et al. Sirt1-ROS-TRAF6 signaling-induced pyroptosis contributes to early injury in ischemic mice[J]. Neurosci Bull, 2020, 36(8): 845-859.
[37]	An P, Xie J, Qiu S, et al. Hispidulin exhibits neuroprotective activities against cerebral ischemia reperfusion injury through suppressing NLRP3-mediated pyroptosis[J]. Life Sci, 2019, 232: 116599.
[38]	Wang L, Negro R, Wu H. TRPM2, linking oxidative stress and Ca2+ permeation to NLRP3 inflammasome activation[J]. Curr Opin Immunol, 2020, 62: 131-135.
[39]	McKenzie BA, Mamik MK, Saito LB, et al. Caspase-1 inhibition prevents glial inflammasome activation and pyroptosis in models of multiple sclerosis[J]. Proc Natl Acad Sci USA, 2018, 115(6): E6065-E6074.
[40]	Xia P, Pan Y, Zhang F, et al. Pioglitazone confers neuroprotection against ischemia-induced pyroptosis due to its inhibitory effects on HMGB-1/RAGE and Rac1/ROS pathway by activating PPAR-γ[J]. Cell Physiol Biochem, 2018, 45(6): 2351-2368.
[41]	Wang H, Chen H, Jin J, et al. Inhibition of the NLRP3 inflammasome reduces brain edema and regulates the distribution of aquaporin-4 after cerebral ischaemia-reperfusion[J]. Life Sci, 2020, 251: 117638.
[42]	Scherz-Shouval R, Shvets E, Elazar Z. Oxidation as a post-translational modification that regulates autophagy[J]. Autophagy, 2007, 3(4): 371-373.
[43]	Nabavi SF, Sureda A, Sanches-Silva A, et al. Novel therapeutic strategies for stroke: the role of autophagy[J]. Crit Rev Clin Lab Sci, 2019, 56: 182-199.

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