Role of nitric oxide and its derivatives in ischemic cerebrovascular disease

doi:10.3969/j.issn.1006-7795.2017.01.014

Abstract

Abstract: Ischemic stroke is the major cause of death and remains as one of the most common causes of disability worldwide. It is well known that cerebral ischemic injury enhances the formation of nitric oxide (NO). It is believed that excessive NO production plays an important role in the development of ischemic brain injury. NO probably contribute to ischemic injury by attacking macromolecules directly, including proteins and lipids, and disrupting mitochondrial function, or indirectly affecting cellular signaling pathways and gene regulation. Excessive production of NO may be neurotoxic, which leads to cascade reactions of excitotoxicity, inflammation and apoptosis. However, NO may also play a neuroprotective role in brain ischemia processes. In this paper, the role of NO and its derivatives in cerebral ischemic injury are reviewed.

Key words: nitric oxide (NO), ischemic stroke, peroxynitrite, N₂O₃

CLC Number:

R743.31

Huang Yuyou, Fang Yalan, Liu Kejian, Zhao Yongmei. Role of nitric oxide and its derivatives in ischemic cerebrovascular disease[J]. Journal of Capital Medical University, 2017, 38(1): 67-71.

0
/ / Recommend

Add to citation manager EndNote|Reference Manager|ProCite|BibTeX|RefWorks

URL: https://journal03.magtech.org.cn/Jweb_sdykdxxb/EN/10.3969/j.issn.1006-7795.2017.01.014

https://journal03.magtech.org.cn/Jweb_sdykdxxb/EN/Y2017/V38/I1/67

References

[1] Liu H, Li J, Zhao F, et al. Nitric oxide synthase in hypoxic or ischemic brain injury[J].Rev Neurosci,2015,26(1):105-117.
[2] Miao J, Huo Y, Lv X, et al. Fast-response and highly selective fluorescent probes for biologic signaling molecule NO based on N-nitrosation of electron-rich aromatic secondary amines[J]. Biomaterials, 2016,78:11-19.
[3] Li H, Liu X, Cui H, et al.Characterization of the mechanism of cytochrome P450 reductase-cytochrome P450-mediatednitric oxide and nitrosothiol generation from organic nitrates[J]. J Biol Chem, 2006, 281(18):12546-12554.
[4] 孙素群,许霖水. 一氧化氮间接作用机制的研究进展[J]. 生理科学进展, 2002,33(2):167-169.
[5] Moro M A, Cárdenas A, Hurtado O, et al. Role of nitric oxide after brain ischaemia[J]. Cell Calcium, 2004,36(3-4):265-275.
[6] Magierowski M, Magierowska K, Kwiecien S, et al. Gaseous mediators nitric oxide and hydrogen sulfide in the mechanism of gastrointestinal integrity, protection and ulcer healing[J]. Molecules, 2015,20(5):9099-9123.
[7] Demicheli V, Moreno D M, Jara G E, et al. Mechanism of the reaction of human manganese superoxide dismutase with peroxynitrite:nitration of critical tyrosine 34[J]. Biochemistry, 2016,55(24):3403-3417.
[8] Carballal S, Bartesaghi S, Radi R. Kinetic and mechanistic considerations to assess the biological fate of peroxynitrite[J].Biochim Biophys Acta, 2014,1840(2):768-780.
[9] Islam B U, Habib S, Ahmad P, et al. Pathophysiological role of peroxynitriteinduced DNA damage in human diseases:aspecial focus on poly(ADP-ribose) polymerase (PARP)[J]. Indian J Clin Biochem, 2015,30(4):368-385.
[10] Roche C J, Cassera M B, Dantsker D, et al. Generating S-nitrosothiols from hemoglobin:mechanisms, conformational dependence, and physiological relevance[J]. J Biol Chem, 2013,288(31):22408-22425.
[11] Eu J P, Liu L, Zeng M, et al. An apoptotic model for nitrosativstress[J]. Biochemitry, 2000,39(5):1040-1047.
[12] Ridnour L A, Thomas D D, Mancardi D, et al. The chemistry of nitrosative stress induced by nitric oxide and reactive nitrogen oxide species. Putting perspective on stressful biological situations[J]. Biol Chem, 2004,385(1):1-10.
[13] Watanabe A, Sasaki T, Yukami T, et al. Serine racemase inhibition induces nitric oxide-mediated neurovascular protection during cerebral ischemia[J]. Neuroscience, 2016,339:139-149.
[14] Oehlschläger S, Albrecht S, Hakenberg O W, et al. Measurement of free radicals and NO by chemiluminescence to identify the reperfusion injury in renal transplantation[J]. Luminescence, 2002,17(2):130-132.
[15] Saito M, Miyagawa I. Real-time monitoring of nitric oxide in ischemia-reperfusion rat kidney[J]. Urol Res, 2000,28(2):141-146.
[16] Lui S L, Chan L Y, Zhang X H, et al. Effect of mycophenolatemofetil on nitric oxide production and inducible nitric oxide synthase gene expression during renal ischaemia-reperfusion injury[J]. Nephrol Dial Transplant, 2001,16(8):1577-1582.
[17] Okamoto M, Tsuchiya K, Kanematsu Y, et al. Nitrite-derived nitric oxide formation following ischemia-reperfusion injury in kidney[J]. Am J Physiol Renal Physiol, 2005,288(1):F182-F187.
[18] Ouyang J, Hong H, Shen C, et al. A novel fluorescent probe for the detection of nitric oxide in vitro and in vivo[J]. Free Rad Biol Med, 2008,45(10):1426-1436.
[19] 周李承,章林慧,梁桂媛,等. 鲁米诺-过氧化氢化学发光法动态监测硝普钠在小鼠体内释放NO过程[J]. 华中科技大学学报,2003,32(4):378-380.
[20] Jain P, David A, Bhatla S C. A novel protocol for detection of nitric oxide in plants[J]. Method Mol Biol, 2016,1424:69-79.
[21] Horn P, Cortese-Krott M M, Amabile N, et al. Circulating microparticles carry a functional endothelial nitric oxide synthase that is decreased in patients with endothelial dysfunction[J]. J Am Heart Assoc, 2012,2(1):e003764.
[22] 杨流海,陈江宁,张峻峰. 新型荧光探针应用于帕金森病模型中NO的检测[J].东南大学学报:医学版, 2014,(5):555-560.
[23] Peng T, Wong N K, Chen X, et al. Correction to "molecular imaging of peroxynitrite with HKGreen-4 in live cells and tissues"[J]. J Am Chem Soc, 2016,18,138(19):6311.
[24] Yuan Z, Liu W, Liu B, et al. Normobarichyperoxia delays and attenuates early nitric oxide production in focal cerebral ischemic rats[J]. Brain Res, 2010,1352:248-254.
[25] 马语曼, 孙琪, 董玉, 等. 硝化应激参与衰老血管内皮功能障碍[J]. 首都医科大学学报, 2015, (6):908-914.
[26] Zhao H, Tao Z, Wang R, et al. MicroRNA-23a-3p attenuates oxidative stress injury in a mouse model of focal cerebral ischemia-reperfusion[J]. Brain Res, 2014,1592:65-72.
[27] Zhao H, Wang R, Tao Z, et al. Activation of T-LAK-cell-originated protein kinasemediatedantioxidation protects against focal cerebral ischemia-reperfusion injury[J]. FEBS J, 2014,281(19):4411-4420.
[28] Vanin A F, Bevers L M, Slama-Schwok A, et al. Nitric oxide synthase reduces nitrite to NO under anoxia[J]. Cell Mol Life Sci, 2007,64(1):96-103.
[29] Yang P S, Lin P Y, Chang C C, et al. Antrodiacamphoratapotentiates neuroprotection against cerebral ischemia in rats via downregulation of iNOS/HO-1/Bax and activated caspase-3 and inhibition of hydroxyl radical formation[J]. Evid Based Complement Alternat Med, 2015,2015:232789.
[30] del Zoppo G, Ginis I, Hallenbeck J M, et al. Inflammation and stroke:putative role for cytokines, adhesion molecules and iNOS in brain response to ischemia[J].Brain Pathol, 2000,10(1):95-112.
[31] Kidd G A, Hong H, Majid A, et al.Inhibition of brain GTP cyclohydrolase I and tetrahydrobiopterin attenuates cerebral infarction via reducing inducible NO synthase and peroxynitrite in ischemic stroke[J]. Stroke, 2005,36(12):2705-2711.
[32] Kim J H, Choi K H, Jang Y J, et al.Electroacupuncture acutely improves cerebral blood flow and attenuates moderate ischemic injury via an endothelial mechanism in mice[J].PLoS One, 2013, 8(2):e56736.
[33] Fujikawa D G.The role of excitotoxic programmed necrosis in acute brain injury[J].Comput Struct Biotechnol J, 2015,13:212-221.
[34] Piazza M, Futrega K, Spratt D E, et al. Structure and dynamics of calmodulin (CaM) bound to nitric oxide synthase peptides:effects of a phosphomimetic CaM mutation[J]. Biochemistry, 2012,51(17):3651-3661.
[35] Zheng L, Ding J, Wang J, et al. Effects and mechanism of action of inducible nitric oxide synthase on apoptosis in a rat model of cerebral ischemia-reperfusion injury[J]. Anat Rec:Hoboken, 2016, 299(2):246-255.
[36] Brown C M, Dela Cruz C D, Yang E, et al.Inducible nitric oxide synthase and estradiol exhibit complementary neuroprotective roles after ischemic brain injury[J]. Exp Neurol, 2008,210(2):782-787.
[37] 邵正凯, 刘爽,王雪峰. 一氧化氮/环磷酸鸟苷信号与蛛网膜下腔出血后脑血管痉挛相关机制的研究进展[J]. 中国脑血管病杂志,2016,13(3):165-168.
[38] 刘云, 高晓莹,戚思华. 缺血后处理脑保护作用的研究进展[J]. 中国脑血管病杂志. 2015,12(3):160-164.