YOPIQ BOSH MIYA JAROHATLAR BILAN KASALLANGAN BEMORLARDA IKKILAMCHI NEYROPROTEKSIYANING PATOGENETIK TAMOYILLARI. (Sharh maqolasi)
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Abstract
yopiq bosh miya jarohati butun dunyo bo‘ylab o‘lim va og‘ir nogironlikning asosiy sababidir. Qurbonlarini davolash va reabilitatsiya qilish turli mamlakatlar byudjetlariga katta ziyon yetkazadi. Psixologik va jismoniy yuk, hayot sifatining pasayishi va sezilarli xarajatlar faqat ushbu bemorlarni boshqarishning qo‘shimcha, yanada murakkab va samarali variantlari zarurligini ta'kidlashi mumkin. Neyroproteksiya kontseptsiyasi ishemiya tomonidan qo‘zg‘atilgan murakkab patofiziologik o‘zgarishlardan foydalangan holda yaxshiroq natijaga erishish vositasi bo‘lib, ko‘plab terapevtik va jarrohlik strategiyalarining markazida bo‘lib kelgan va shunday bo‘lib qoladi. Eksitotoksiklik, apoptoz va oksidlovchi stressdan yallig‘lanishgacha bo‘lgan YBMJning turli mexanizmlarini keltirib chiqaradigan bir necha turdagi asoratlar o‘rganildi va ularning aksariyati klinik bosqichda umidsizlikka olib keldi va zararning har bir bosqichida zararning u yoki bu yo‘lini oldini olish yoki oqibatlarni minimallashtirish uchun himoya - neyroproteksiya qilish kerak. Bu esa neyroproteksiyaning muhim davolash taktikasi bo‘lib qolayotganini ko‘rsatadi. Ushbu sharhda klinik jihatdan o‘rganilgan neyroproteksiya usullari, ularning mexanizmlari, natijalari neyroproteksiyaning potentsial maqsadlari va maqsadli davolash usullari haqida qisqacha ma'lumot berilgan.
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References
Avakov V.E., Ibragimov N.K., Murotov TM.N., Kenjaev L.T. Comparative characteristics of the effects of hyperosmolar therapy in patients with craniocerebral trauma.Вестник Ташкенской медидсниской академии 2018 № 3 97-101 с.
Gaytur E.I., Potapov A.A. et al. The influence of arterial hypotension on the course and outcomes of severe traumatic brain injury // Resuscitation at the turn of the 21st century. – M., 2006. – 126 p.
Kahle K.T., Simard J.M. et al. Molecular mechanisms of ischemic cerebral edema: Role of electroneutral ion transport // Physiology (Bethesda). – 2009. – Vol. 24. – Р. 257-265.
Kamel H., Navi B.B. et al. Hypertonic salineversus mannitol for the treatment of elevated intracranial pressure: a metaanalysis of randomized clinical trials // Crit. Care Med. – 2011. Vol. 39. – Р. 554-559
Kaufmann A.M., Cardoso E.R. Aggravation of vasogenic cerebral edema by multiple-dose mannitol // J. Neurosurg. – 1992. – Vol. 77. – Р. 584-589.
Kerwin A.J., Schinco M.A. et al. The use of 23.4% hypertonic saline for the management of elevatedintracranial pressure in patients with severe traumatic brain injury: a pilot study // J. Trauma. – 2009. – Vol. 67. – Р. 277-282.
Zadori D, Klivenyi P, Szalardy L, Fulop F, Toldi J, Vecsei L. Mitochondrial Disturbances, Excitotoxicity, Neuroinflammation and Kynurenines: Novel Therapeutic Strategies for Neurodegenerative Disorders. J Neurol Sci. 2012;322:187-91.
Majid A. Neuroprotection in Stroke: Past, Present, and Future. ISRN Neurol. 2014;2014:515716.
Krylov V.V. Surgery of severe traumatic brain injury. Under the general editorship of Krylova V.V. Moscow, 2019. 647 p.
Donnan GA, Davis SM, Parsons MW, Ma H, Dewey HM, Howells DW. How to Make Better Use of Thrombolytic Therapy in Acute Ischemic Stroke. Nat Rev Neurol. 2011;7:400-9.
Shuaib A, Hussain MS. The Past and Future of Neuroprotection in Cerebral Ischaemic Stroke. Eur Neurol. 2008;59:4-14.
Fisher M. New Approaches to Neuroprotective Drug Development. Stroke. 2011;42:S24-7.
Wahlgren NG, Ahmed N. Neuroprotection in Cerebral Ischaemia: Facts and Fancies--the Need for New Approaches. Cerebrovasc Dis.2004;17 Suppl 1:153-66.
Deb P, Sharma S, Hassan KM. Pathophysiologic Mechanisms of Acute Ischemic Stroke: An Overview with Emphasis on Therapeutic Significance Beyond Thrombolysis. Pathophysiology.2010;17:197-218.
Jablonska A, Lukomska B. Stroke Induced Brain Changes: Implications for Stem Cell Transplantation. Acta Neurobiol Exp (Wars). 2011;71:74-85.
Yang DD, Kuan CY, Whitmarsh AJ, Rincon M, Zheng TS, Davis RJ, et al. Absence of Excitotoxicity-Induced Apoptosis in the Hippocampus of Mice Lacking the Jnk3 Gene. Nature. 1997;389:865- 70.
Ankarcrona M, Dypbukt JM, Bonfoco E, Zhivotovsky B, Orrenius S, Lipton SA, et al. Glutamate-Induced Neuronal Death: A Succession of Necrosis or Apoptosis Depending on Mitochondrial Function. Neuron. 1995;15:961-73.
Dutta R, Trapp BD. Mechanisms of Neuronal Dysfunction and Degeneration in Multiple Sclerosis. Prog Neurobiol. 2011;93:1-12.
Jaiswal MK, Zech WD, Goos M, Leutbecher C, Ferri A, Zippelius A, et al. Impairment of Mitochondrial Calcium Handling in Mtsod1 Cell Culture Model of Motoneuron Disease. BMC Neurosci. 2009;10:64.
Manev H, Favaron M, Guidotti A, Costa E. Delayed Increase of Ca2+ Influx Elicited by Glutamate: Role in Neuronal Death. Mol Pharmacol. 1989;36:106-12.
Kaur H, Prakash A, Medhi B. Drug Therapy in Stroke: From Preclinical to Clinical Studies. Pharmacology. 2013;92:324-34.
White BC, Sullivan JM, DeGracia DJ, O'Neil BJ, Neumar RW, Grossman LI, et al. Brain Ischemia and Reperfusion: Molecular Mechanisms of Neuronal Injury. J Neurol Sci. 2000;179:1-33.
Stavrovskaya IG, Kristal BS. The Powerhouse Takes Control of the Cell: Is the Mitochondrial Permeability Transition a Viable Therapeutic Target against Neuronal Dysfunction and Death? Free Radic Biol Med. 2005;38:687-97.
Kristian T, Siesjo BK. Calcium-Related Damage in Ischemia. Life Sci. 1996;59:357-67.
Zhang J, Yang J, Zhang C, Jiang X, Zhou H, Liu M. Calcium Antagonists for Acute Ischemic Stroke. Cochrane Database Syst Rev.2012:CD001928.
Nowak L, Bregestovski P, Ascher P, Herbet A, Prochiantz A. Magnesium Gates Glutamate-Activated Channels in Mouse Central Neurones. Nature. 1984;307:462-5.
Izumi Y, Roussel S, Pinard E, Seylaz J. Reduction of Infarct Volume by Magnesium after Middle Cerebral Artery Occlusion in Rats. J Cereb Blood Flow Metab. 1991;11:1025-30.
Muir KW, Lees KR, Ford I, Davis S, Intravenous Magnesium Efficacy in Stroke Study I. Magnesium for Acute Stroke (Intravenous Magnesium Efficacy in Stroke Trial): Randomised Controlled Trial. Lancet. 2004;363:439-45.
Saver JL, Kidwell C, Eckstein M, Starkman S, Investigators FMPT. Prehospital Neuroprotective Therapy for Acute Stroke: Results of the Field Administration of Stroke Therapy-Magnesium (Fast-Mag) Pilot Trial. Stroke. 2004;35:e106-8.
Grupke S, Hall J, Dobbs M, Bix GJ, Fraser JF. Understanding History, and Not Repeating It. Neuroprotection for Acute Ischemic Stroke: From Review toPreview. Clin Neurol Neurosurg. 2015;129:1- 9.
Lehmann J, Hutchison AJ, McPherson SE, Mondadori C, Schmutz M, et al. Cgs 19755, a Selective and Competitive N-Methyl-D-Aspartate-Type Excitatory Amino Acid Receptor Antagonist. J Pharmacol Exp Ther. 1988;246:6575.
Miyabe M, Kirsch JR, Nishikawa T, Koehler RC, Traystman RJ. Comparative Analysis of Brain Protection by N-Methyl-D-Aspartate Receptor Antagonists after Transient Focal Ischemia in Cats. Crit Care Med. 1997;25:1037-43.
Simon R, Shiraishi K. N-Methyl-D-Aspartate Antagonist Reduces Stroke Size and Regional Glucose Metabolism. Ann Neurol. 1990;27:606-11.
Grotta J, Clark W, Coull B, Pettigrew LC, Mackay B, Goldstein LB, et al. Safety and Tolerability of the Glutamate Antagonist Cgs 19755 (Selfotel) in Patients with Acute Ischemic Stroke. Results of a Phase Iia Randomized Trial. Stroke.1995;26:602-5.
Davis SM, Lees KR, Albers GW, Diener HC, Markabi S, Karlsson G, et al. Selfotel in Acute Ischemic Stroke : Possible Neurotoxic Effects of an Nmda Antagonist.Stroke.2000;31:347-54.
Jain KK. The Handbook of Neuroprotection. 1. ed. Totowa, NJ: Springer Science+Business Media, LLC; 2011.
Suzuki M, Sasamata M, Miyata K. Neuroprotective Effects of Ym872 Coadministered with T-Pa in a Rat Embolic Stroke Model. Brain Res. 2003;959:169-72.
Furukawa T, Hoshino S, Kobayashi S, Asakura T, Takahashi M, Atsumi T, et al. The Glutamate Ampa Receptor Antagonist, Ym872, Attenuates Cortical Tissue Loss, Regional Cerebral Edema, and Neurological Motor Deficits after Experimental Brain Injury in Rats. J Neurotrauma. 2003;20:269-78.
Farooqui AA. Neurochemical Aspects of Neurotraumatic and Neurodegenerative Diseases. New York, NY: Springer Science+Business Media, LLC;2010.
Garcia JH, Yoshida Y, Chen H, Li Y, Zhang ZG, Lian J, et al. Progression from Ischemic Injury to Infarct Following Middle Cerebral Artery Occlusion in the Rat. Am J Pathol. 1993;142:623-35.
Broughton BR, Reutens DC, Sobey CG. Apoptotic Mechanisms after Cerebral Ischemia. Stroke. 2009;40:e331-9.
Li Y, Chopp M, Jiang N, Yao F, Zaloga C. Temporal Profile of in Situ DNA Fragmentation after Transient Middle Cerebral Artery Occlusion in the Rat. J Cereb Blood Flow Metab. 1995;15:389-97.
Li Y, Chopp M, Jiang N, Zhang ZG, Zaloga C. Induction of DNA Fragmentation after 10 to 120 Minutes of Focal Cerebral Ischemia in Rats. Stroke. 1995;26:1252-7; discussion 7-8.
Mattson MP, Culmsee C, Yu ZF. Apoptotic and Antiapoptotic Mechanisms in Stroke. Cell Tissue Res. 2000;301:173-87.
MacManus JP, Buchan AM. Apoptosis after Experimental Stroke: Fact or Fashion? J Neurotrauma. 2000;17:899-914.
Elliott S, Sinclair AM. The Effect of Erythropoietin on Normal and Neoplastic Cells. Biologics. 2012;6:163-89.
Chong ZZ, Kang JQ, Maiese K. Erythropoietin Is a Novel Vascular Protectant through Activation of Akt1 and Mitochondrial Modulation of Cysteine Proteases. Circulation. 2002;106:2973-9.
Digicaylioglu M. Erythropoietin in Stroke: Quo Vadis. Expert Opin Biol Ther. 2010;10:937-49.
Wen TC, Sadamoto Y, Tanaka J, Zhu PX, Nakata K, Ma YJ, et al. Erythropoietin Protects Neurons against Chemical Hypoxia and Cerebral Ischemic Injury by up-Regulating Bcl-Xl Expression. J Neurosci Res. 2002;67:795-803.
Ehrenreich H, Hasselblatt M, Dembowski C, Cepek L, Lewczuk P, Stiefel M, et al. Erythropoietin Therapy for Acute Stroke Is Both Safe and Beneficial. Mol Med.2002;8:495-505.
Ehrenreich H, Weissenborn K, Prange H, Schneider D, Weimar C, Wartenberg K, et al. Recombinant Human Erythropoietin in the Treatment of Acute Ischemic Stroke. Stroke. 2009;40:e647-56.
Heiss WD, Brainin M, Bornstein NM, Tuomilehto J, Hong Z, Cerebrolysin Acute Stroke Treatment in Asia I. Cerebrolysin in Patients with Acute Ischemic Stroke in Asia: Results of a DoubleBlind, Placebo-Controlled Randomized Trial. Stroke. 2012;43:630-6.
Menon PK, Muresanu DF, Sharma A, Mossler H, Sharma HS. Cerebrolysin, a Mixture of Neurotrophic Factors Induces Marked Neuroprotection in Spinal Cord Injury Following Intoxication of Engineered Nanoparticles from Metals. CNS Neurol Disord Drug Targets. 2012;11:40-9.
Hartbauer M, Hutter-Paier B, Skofitsch G, Windisch M. Antiapoptotic Effects of the Peptidergic Drug Cerebrolysin on Primary Cultures of Embryonic Chick Cortical Neurons. J Neural Transm (Vienna). 2001;108:459-73.
Zhang L, Chopp M, Meier DH, Winter S, Wang L, Szalad A, et al. Sonic Hedgehog Signaling Pathway Mediates CerebrolysinImproved Neurological Function after Stroke. Stroke. 2013;44:1965-
Gutmann B, Hutter-Paier B, Skofitsch G, Windisch M, Gmeinbauer R. In Vitro Models of Brain Ischemia: The Peptidergic Drug Cerebrolysin Protects Cultured Chick Cortical Neurons from Cell Death. Neurotox Res.2002;4:59-65.
Masliah E, Diez-Tejedor E. The Pharmacology of Neurotrophic Treatment with Cerebrolysin: Brain Protection and Repair to Counteract Pathologies of Acute and Chronic Neurological Disorders. Drugs Today (Barc). 2012;48 Suppl A:3-24.
Muresanu DF, Heiss WD, Hoemberg V, Bajenaru O, Popescu CD, Vester JC, et al. Cerebrolysin and Recovery after Stroke (Cars): A Randomized, Placebo-Controlled, Double-Blind, Multicenter Trial. Stroke. 2016;47:151-9.
Zhang C, Chopp M, Cui Y, Wang L, Zhang R, Zhang L, et al. Cerebrolysin Enhances Neurogenesis in the Ischemic Brain and Improves Functional Outcome after Stroke. J Neurosci Res. 2010;88:3275-81.
Amiri-Nikpour MR, Nazarbaghi S, Ahmadi-Salmasi B, Mokari T, Tahamtan U, Rezaei Y. Cerebrolysin Effects on Neurological Outcomes and Cerebral Blood Flow in Acute Ischemic Stroke. Neuropsychiatr Dis Treat. 2014;10:2299-306.
Chamorro A, Hallenbeck J. The Harms and Benefits of Inflammatory and Immune Responses in Vascular Disease. Stroke. 2006;37:291-3.
Barone FC, Feuerstein GZ. Inflammatory Mediators and Stroke: New Opportunities for Novel Therapeutics. J Cereb Blood Flow Metab.1999;19:819-34.
Becker KJ. Inflammation and Acute Stroke. Curr Opin Neurol. 1998;11:45-9
Stanimirovic DB, Wong J, Shapiro A, Durkin JP. Increase in Surface Expression of Icam-1, Vcam-1 and E-Selectin in Human Cerebromicrovascular Endothelial Cells Subjected to Ischemia-Like Insults. Acta Neurochir Suppl. 1997;70:12-6.
Danton GH, Dietrich WD. Inflammatory Mechanisms after Ischemia and Stroke. J Neuropathol Exp Neurol. 2003;62:127-36.
Basu A, Lazovic J, Krady JK, Mauger DT, Rothstein RP, Smith MB, et al. Interleukin-1 and the Interleukin-1 Type 1 Receptor Are Essential for the Progressive Neurodegeneration That Ensues Subsequent to a Mild Hypoxic/Ischemic Injury. J Cereb Blood Flow Metab. 2005;25:17-29.
Peberdy MA, Callaway CW, Neumar RW, Geocadin RG, Zimmerman JL, Donnino M, et al. Part 9: Post-Cardiac Arrest Care: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2010;122:S768-86.
Polderman KH. Application of Therapeutic Hypothermia in the Icu: Opportunities and Pitfalls of a Promising Treatment Modality. Part 1: Indications and Evidence. Intensive Care Med. 2004;30:556-75.
Milde LN. Clinical Use of Mild Hypothermia for Brain Protection: A Dream Revisited. J Neurosurg Anesthesiol. 1992;4:211-5.
Ehrlich MP, McCullough JN, Zhang N, Weisz DJ, Juvonen T, Bodian CA, et al. Effect of Hypothermia on Cerebral Blood Flow and Metabolism in the Pig. Ann Thorac Surg. 2002;73:191-7.
Erecinska M, Thoresen M, Silver IA. Effects of Hypothermia on Energy Metabolism in Mammalian Central Nervous System. J Cereb Blood Flow Metab. 2003;23:513-30.
Polderman KH. Mechanisms of Action, Physiological Effects, and Complications of Hypothermia. Crit Care Med. 2009;37:S186-202.
Busto R, Dietrich WD, Globus MY, Ginsberg MD. Postischemic Moderate Hypothermia Inhibits Ca1 Hippocampal Ischemic Neuronal Injury. Neurosci Lett. 1989;101:299-304.
Baldwin WA, Kirsch JR, Hurn PD, Toung WS. Hypothermic Cerebral Reperfusion and Recovery from Ischemia. Am J Physiol.1991;261:H774 81.
Wang GJ, Deng HY, Maier CM, Sun GH, Yenari MA. Mild Hypothermia Reduces Icam-1 Expression, Neutrophil Infiltration and Microglia/Monocyte Accumulation Following Experimental Stroke. Neuroscience. 2002;114:1081-90.
Perrone S, Szabo M, Bellieni CV, Longini M, Bango M, Kelen D, et al. Whole Body Hypothermia and Oxidative Stress in Babies with Hypoxic-Ischemic Brain Injury. Pediatr Neurol. 2010;43:236-40.
Meybohm P, Gruenewald M, Zacharowski KD, Albrecht M, Lucius R, Fosel N, et al. Mild Hypothermia Alone or in Combination with Anesthetic Post-Conditioning Reduces Expression of Inflammatory Cytokines in the Cerebral Cortex of Pigs after Cardiopulmonary Resuscitation. Crit Care. 2010;14:R21.
Choi JS, Park J, Suk K, Moon C, Park YK, Han HS. Mild Hypothermia Attenuates Intercellular Adhesion Molecule-1 Induction Via Activation of Extracellular Signal-Regulated Kinase-1/2 in a Focal Cerebral Ischemia Model. Stroke Res Treat. 2011;2011:846716.
Maier K, Merkler D, Gerber J, Taheri N, Kuhnert AV, Williams SK, et al. Multiple Neuroprotective Mechanisms of Minocycline in Autoimmune Cns Inflammation. Neurobiol Dis. 2007;25:514-25.
Tikka TM, Vartiainen NE, Goldsteins G, Oja SS, Andersen PM, Marklund SL, et al. Minocycline Prevents Neurotoxicity Induced by Cerebrospinal Fluid from Patients with Motor Neurone Disease. Brain. 2002;125:722-31.
Tikka TM, Koistinaho JE. Minocycline Provides Neuroprotection against N-Methyl-D-Aspartate Neurotoxicity by Inhibiting Microglia. J Immunol. 2001;166:7527-33.
Brundula V, Rewcastle NB, Metz LM, Bernard CC, Yong VW. Targeting Leukocyte Mmps and Transmigration: Minocycline as a Potential Therapy for Multiple Sclerosis. Brain. 2002;125:1297-308.
Wang X, Zhu S, Drozda M, Zhang W, Stavrovskaya IG, Cattaneo
E, et al. Minocycline Inhibits Caspase-Independent and –Dependent Mitochondrial Cell Death Pathways in Models of Huntington's Disease. Proc Natl Acad Sci U S A. 2003;100:10483-7.
Chen M, Ona VO, Li M, Ferrante RJ, Fink KB, Zhu S, et al. Minocycline Inhibits Caspase-1 and Caspase-3 Expression and Delays Mortality in a Transgenic Mouse Model of Huntington Disease. Nat Med. 2000;6:797-801.
Yrjanheikki J, Tikka T, Keinanen R, Goldsteins G, Chan PH, Koistinaho J. A Tetracycline Derivative, Minocycline, Reduces Inflammation and Protects against Focal Cerebral Ischemia with a Wide Therapeutic Window. Proc Natl Acad Sci U SA.1999;96:13496-500.
Yang F, Zhou L, Wang D, Wang Z, Huang QY. Minocycline Ameliorates Hypoxia-Induced Blood–Brain Barrier Damage by Inhibition of Hif-1α through Sirt-3/Phd-2 Degradation Pathway. Neuroscience. 2015;304:250-9.
Kim DK, Rordorf G, Nemenoff RA, Koroshetz WJ, Bonventre JV. Glutamate Stably Enhances the Activity of Two Cytosolic Forms of Phospholipase A2 in Brain Cortical Cultures. Biochem J. 1995;310 (Pt1):83-90.
Katsuki H, Okuda S. Arachidonic Acid as a Neurotoxic and Neurotrophic Substance. Prog Neurobiol.1995;46:607-36.
Seidl SE, Potashkin JA. The Promise of Neuroprotective Agentsin Parkinson's Disease. Front Neurol. 2011;2:68.
Dunnett SB, Bjorklund A. Prospects for New Restorative and
Neuroprotective Treatments in Parkinson's Disease. Nature. 1999;399:A32-9.
Chan PH. Reactive Oxygen Radicals in Signaling and Damage in the Ischemic Brain. J Cereb Blood Flow Metab. 2001;21:2-14.
Liu T, Bitan G. Modulating Self-Assembly of Amyloidogenic Proteins as a Therapeutic Approach for Neurodegenerative Diseases: Strategies and Mechanisms. ChemMedChem. 2012;7:359-74.
Pradeep H, Diya JB, Shashikumar S, Rajanikant GK. Oxidative Stress--Assassin Behind the Ischemic Stroke. Folia Neuropathol. 2012;50:219-30.
Secades JJ, Alvarez-Sabin J, Rubio F, Lozano R, Davalos A, Castillo J, et al. Citicoline in Intracerebral Haemorrhage: A DoubleBlind, Randomized, Placebo Controlled, Multi-Centre Pilot Study. Cerebrovasc Dis. 2006;21:380-5.
Cho HJ, Kim YJ. Efficacy and Safety of Oral Citicoline in Acute Ischemic Stroke: Drug Surveillance Study in 4,191 Cases. Methods Find Exp Clin Pharmacol. 2009;31:171-6.
Alvarez-Sabin J, Ortega G, Jacas C, Santamarina E, Maisterra O, Ribo M, et al. Long-Term Treatment with Citicoline May Improve Poststroke Vascular Cognitive Impairment. Cerebrovasc Dis. 2013;35:146-54.
IL GC, Wurtman RJ. Enhancement by Cytidine of Membrane Phospholipid Synthesis. J Neurochem. 1992;59:338-43.
Schabitz WR, Weber J, Takano K, Sandage BW, Locke KW, Fisher M. The Effects of Prolonged Treatment with Citicoline in Temporary Experimental Focal Ischemia. J Neurol Sci. 1996;138:21-5.
Hurtado O, Pradillo JM, Fernandez-Lopez D, Morales JR, Sobrino T, Castillo J, et al. Delayed Post-Ischemic Administration of Cdp-Choline Increases Eaat2 Association to Lipid Rafts and Affords Neuroprotection in Exp Stroke. Neurobiol Dis. 2008;29:123-31.
Adibhatla RM, Hatcher JF, Dempsey RJ. Citicoline: Neuroprotective Mechanisms in Cerebral Ischemia. J Neurochem. 2002;80:12-23.
Rao AM, Hatcher JF, Dempsey RJ. Cdp-Choline: Neuroprotection in Transient Forebrain Ischemia of Gerbils. J Neurosci Res. 1999;58:697-705.
De La Cruz JP, Villalobos MA, Cuerda MA, Guerrero A, Gonzalez-Correa JA, Sanchez De La Cuesta F. Effects of S-AdenosylL-Methionine on Lipid Peroxidation and Glutathione Levels in Rat Brain Slices Exposed to Reoxygenation after Oxygen-Glucose Deprivation. Neurosci Lett. 2002;318:103-7.
Ramazanova Z.F., Avakov V.E., Ibragimov N.K., Muralimova R.S., Boymurodov H. Efficiency of complex neuroprotection with the use of the drug Edaravone (Radixoba-Tsommer) Tashkent Medical Academy Department of Anesthesiology and Resuscitation.
He WF, Zhou WS, Hu ZP. Chinese Herbal Extract Dl-3nButylphthalide a Commonly Used Drug for the Treatment of Ischemic Stroke as a Novel Therapeutic Approach to Treat Neurodegenerative Diseases. Neural Regeneration Research. 2011;6:2773-8.
Zhao W, Luo C, Wang J, Gong J, Li B, Gong Y, et al. 3-NButylphthalide Improves Neuronal Morphology after Chronic Cerebral Ischemia. Neural Regen Res.2014;9:719-26.
Sun B, Feng MJ, Tian XY, Lu XW, Zhang YY, Ke XJ, et al. Dl- 3-N-Butylphthalide Protects Rat Bone Marrow Stem Cells against Hydrogen Peroxide-Induced Cell Death through Antioxidation and Activation of Pi3k-Akt Pathway. Neuroscience Letters. 2012;516:247-52.
Chao J, Chao L. Experimental Therapy with Tissue Kallikrein against Cerebral Ischemia. Front Biosci. 2006;11:1323-7.
Zhang C, Tao W, Liu M, Wang D. Efficacy and Safety of
Human Urinary Kallidinogenase Injection for Acute Ischemic Stroke: A Systematic Review. J Evid Based Med. 2012;5:31-9.
Li C, Zha OG, He QY, Wu YZ, Wang TS, Teng JF. Study on
the Clinical Efficacy of Human Urinary Kalllikrein in the Treatment of Acute Cerebral Infarction According to Toast Classification. Pak J Pharm Sci. 2015;28:1505-10.
Miao J, Deng F, Zhang Y, Xie HY, Feng JC. Exogenous Human Urinary Kallidinogenase Increases Cerebral Blood Flow in Patients with Acute Ischemic Stroke. Neurosci (Riyadh). 2016;21:126-30.
Li J, Chen Y, Zhang X, Zhang B, Zhang M, Xu Y. Human
Urinary Kallidinogenase Improves Outcome of Stroke Patients by Shortening Mean Transit Time of Perfusion Magnetic Resonance Imaging. J Stroke Cerebrovasc Dis. 2015;24:1730-7.
Han L, Li J, Chen Y, Zhang M, Qian L, Chen Y, et al. Human Urinary Kallidinogenase Promotes Angiogenesis and Cerebral Perfusion in Experimental Stroke. PLoS One. 2015;10:e0134543.
Zhao L, Zhao Y, Wan Q, Zhang H. Urinary Kallidinogenase for the Treatment of Cerebral Arterial Stenosis. Drug Des Devel Ther. 2015;9:5595-600.
Liu L, Zhang R, Liu K, Zhou H, Tang Y, Su J, et al. Tissue Kallikrein Alleviates Glutamate-Induced Neurotoxicity by Activating Erk1. Journal of Neuroscience Research. 2009;87:3576-90.