PL EN


Preferences help
enabled [disable] Abstract
Number of results
2013 | 13 | 1 | 16–23
Article title

Procesy patologiczne w mózgu podczas jego niedokrwienia

Content
Title variants
EN
Pathological processes in the brain during ischaemia
Languages of publication
PL
Abstracts
EN
Stroke to the present is one of the most common causes of death and permanent disability. Ischemic stroke (ischemic stroke called IS) is not only a dangerous disease because of its high mortality rate, but also because of a disability in patients who do survive, which represents approximately 76% of cases. It is a heterogeneous disease entity, which is a set of symptoms caused by focal ischemia or bleeding into the brain tissue caused by a wide variety of reasons. There are two types of strokes: haemorrhagic and ischemic. Haemorrhagic strokes account for 20% of all strokes, the other 80% are ischemic strokes. Stroke is a systemic disease, mainly resulting from vascular pathology. It plays a huge role in atherosclerosis and the mechanisms involved. The disease process affects the whole of the body, not just the cerebral vessels. From the point of view of pathological, ischemic stroke is the rapidly developing neurodegenerative process that leads to cell death. This disease is beyond the vascular damage, induces cell-molecular immune response to central nervous system and the vascular system, aimed at the development of the inflammatory response. The activated cells of the brain and vascular cells are involved in the synthesis of various molecules, among others. cytokines, chemokines, adhesion molecules and inflammatory enzymes. Continues to grow numerous reports confirming the importance of inflammatory factors in the development of ischemic stroke. In this process, the blood-brain barrier plays an important role. At the cellular level it is the main line of microglia immune surveillance of the central nervous system, which is responsible for the induction of the inflammatory response in stroke. In stroke, a sudden change in the expression of cytokines proceeds, which reveal the neurodegenerative effects of inflammatory cytokines and anti-inflammatory cytokines neuroprotective effect. Processes occurring in the brain during ischemia are very complicated and is not involved in a number of factors.
PL
Udar mózgu (stroke) jest obecnie jedną z najczęstszych przyczyn zgonów i trwałego kalectwa. Udar niedokrwienny mózgu (ischaemic stroke, IS) jest niebezpieczną chorobą nie tylko ze względu na dużą śmiertelność, ale również z powodu niepełnosprawności u pacjentów, którzy go przeżywają (około 76% przypadków). Jest to niejednorodna jednostka chorobowa, będąca zespołem objawów ogniskowych powstałych w wyniku niedokrwienia lub krwotoku do tkanki mózgowej spowodowanych wieloma różnymi przyczynami. Rozróżniamy dwa typy udarów mózgowych: krwotoczne i niedokrwienne. Udary krwotoczne stanowią 15% wszystkich udarów, pozostałe 80% to udary niedokrwienne. Udar mózgu jest chorobą ogólnoustrojową, głównie wynikającą z patologii naczyniowej. Ogromną rolę odgrywa tu miażdżyca i mechanizmy z nią związane. Proces chorobowy dotyczy całego organizmu, a nie tylko naczyń mózgowych. Z punktu widzenia patologii udar niedokrwienny mózgu jest dynamicznie rozwijającym się procesem neurodegeneracyjnym, który prowadzi do śmierci komórek (cell death). Oprócz uszkodzenia naczyniopochodnego choroba ta indukuje komórkowo-molekularną odpowiedź immunologiczną ośrodkowego układu nerwowego i układu naczyniowego, ukierunkowaną na rozwój reakcji zapalnej. Aktywowane komórki mózgu, a także komórki układu naczyniowego zaangażowane są w syntezę różnych molekuł, m.in. cytokin, chemokin, cząsteczek adhezyjnych oraz enzymów prozapalnych. Ciągle rośnie liczba doniesień potwierdzających duże znaczenie czynników zapalnych w rozwoju udaru niedokrwiennego mózgu. W procesie tym znaczącą rolę odgrywa bariera krew-mózg. Na poziomie komórkowym mikroglej stanowi główną linię nadzoru immunologicznego nad ośrodkowym układem nerwowym, odpowiedzialną za indukcję reakcji zapalnej w udarze mózgu. W udarze mózgu następuje gwałtowna zmiana ekspresji cytokin, które ujawniają neurodegeneracyjny efekt cytokin prozapalnych oraz neuroprotekcyjny efekt cytokin antyzapalnych. Procesy zachodzące w mózgu podczas jego niedokrwienia są bardzo skomplikowane i wiele czynników jest w nie zaangażowanych.
Discipline
Year
Volume
13
Issue
1
Pages
16–23
Physical description
References
  • 1. Whisnant J.P., Basford J.R., Bernstein E.F. i wsp.: Special report from the National Institute of Neurological Disorders and Stroke. Classification of cerebrovascular diseases III. Stroke 1990; 21: 637–676.
  • 2. Warlow C., Sudlow C., Dennis M. i wsp.: Stroke. Lancet 2003; 362: 1211–1224.
  • 3. Adams H.P. Jr, Bendixen B.H., Kappelle L.J. i wsp.: Classification of subtype of acute ischemic stroke. Definitions for use in a multicenter clinical trial. TOAST. Trial of Org 10172 in Acute Stroke Treatment. Stroke 1993; 24: 35–41.
  • 4. Goldstein L.B., Jones M.R., Matchar D.B. i wsp.: Improving the reliability of stroke subgroup classification using the Trial of ORG 10172 in Acute Stroke Treatment (TOAST) criteria. Stroke 2001; 32: 1091–1098.
  • 5. Ryglewicz D.: Epidemiologia udaru mózgu. W: Szczudlik A., Członkowska A., Kwieciński H., Słowik A. (red.): Udar mózgu. Wydawnictwo Uniwersytetu Jagiellońskiego, Kraków 2007: 85–95.
  • 6. Chan P.H.: Role of oxidants in ischemic brain damage. Stroke 1996; 27: 1124–1129.
  • 7. Lee J.M., Zipfel G.J., Choi D.W.: The changing landscape of ischaemic brain injury mechanisms. Nature 1999; 399 (6738 supl.): A7–A14.
  • 8. McIlvoy L.H.: The effect of hypothermia and hyperthermia on acute brain injury. AACN Clin. Issues 2005: 16: 488–500.
  • 9. Iadecola C., Alexander M.: Cerebral ischemia and inflammation. Curr. Opin. Neurol. 2001; 14: 89–94.
  • 10. Emerich D.F., Dean R.L., Bartus R.T.: The role of leukocytes following cerebral ischemia: pathogenic variable or bystander reaction to emerging infarct? Exp. Neurol. 2002; 173: 168–181.
  • 11. Nilupul P.M., Ma H.K., Arawaka S. i wsp.: Inflammation following stroke. J. Clin. Neurosci. 2006; 13: 1–8.
  • 12. Dirnagl U., Iadecola C., Moskowitz M.A.: Pathobiology of ischaemic stroke: an integrated view. Trends Neurosci. 1992; 22: 391–397.
  • 13. Pardridge W.M.: The blood-brain barrier: bottleneck in brain drug development. NeuroRx 2005; 2: 3–14.
  • 14. Schlachetzki F., Zhang Y., Boado R.J., Pardridge W.M.: Gene therapy of the brain: the trans-vascular approach. Neurology 2004; 62: 1275–1281.
  • 15. Pardridge W.M.: Blood-brain barrier genomics and the use of endogenous transporters to cause drug penetration into the brain. Curr. Opin. Drug. Discov. Devel. 2003; 6: 683–691.
  • 16. Pardridge W.M.: Blood-brain barrier delivery. Drug Discov. Today 2007; 12: 54–61.
  • 17. Abbott N.J.: Dynamics of CNS barriers: evolution, differentiation, and modulation. Cell Mol. Neurobiol. 2005; 25: 5–23.
  • 18. Abbott N.J., Rönnbäck L., Hansson E.: Astrocyte-endothelial interactions at the blood-brain barrier. Nat. Rev. Neurosci. 2006; 7: 41–53.
  • 19. Anthony D., Dempster R., Fearn S. i wsp.: CXC chemokines generate age-related increases in neutrophil-mediated brain inflammation and blood-brain barrier breakdown. Curr Biol. 1998; 8: 923–926.
  • 20. Farkas G., Márton J., Nagy Z. i wsp.: Experimental acute pancreatitis results in increased blood-brain barrier permeability in the rat: a potential role for tumor necrosis factor and interleukin 6. Neurosci. Lett. 1998; 242: 147–150.
  • 21. Kim K.S., Wass C.A., Cross A.S.: Blood-brain barrier permeability during the development of experimental bacterial meningitis in the rat. Exp. Neurol. 1997; 145: 253–257.
  • 22. Huber J.D., Egleton R.D., Davis T.P.: Molecular physiology and pathophysiology of tight junctions in the blood-brain barrier. Trends Neurosci. 2001; 24: 719–725.
  • 23. Langford D., Masliah E.: Crosstalk between components of the blood brain barrier and cells of the CNS in microglial activation in AIDS. Brain Pathol. 2001; 11: 306–312.
  • 24. Kato H., Walz W.: The initiation of the microglia response. Brain Pathol. 2000; 10: 137–143.
  • 25. Allan S., Stock C.: Cytokines in stroke. Ernst Schering Res. Foun. Workshop 2004; 47: 39–66.
  • 26. Banks W.A.: Blood-brain barrier transport of cytokines: a mechanism for neuropathology. Curr. Pharm. Des. 2005; 11: 973–984.
  • 27. De Simoni M.G.: Two-way communication pathways between the brain and the immune system. Neurosci. Res. Common. 1997; 21: 163–172.
  • 28. Emsley H.C., Tyrrell P.J.: Inflammation and infection in clinical stroke. J. Cereb. Blood Flow. Metab. 2002; 22: 1399–1419.
  • 29. Cartier L., Hartley O., Dubois-Dauphin M., Krause K.H.: Chemokine receptors in the central nervous system: role in the brain inflammation and neurodegenerative diseases. Brain Res. Brain Res. Rev. 2005; 48: 16–42.
  • 30. Losy J., Zaremba J.: Monocyte chemoattractant protein-1 is increased in the cerebrospinal fluid of patients with ischemic stroke. Stroke 2001; 32: 2695–2696.
  • 31. Arakelyan A., Petrkova J., Hermanova Z. i wsp.: Serum levels of the MCP-1 chemokine in patients with ischemic stroke and myocardial infarction. Mediators Inflamm. 2005; 2005: 175–179.
  • 32. Hughes P.M., Allegrini P.R., Rudin M.: Monocyte chemoattractant protein-1 deficiency is protective in a murine stroke model. J. Cereb. Blood Flow. Metab. 2002; 22: 308–317.
  • 33. Dimitrijevic O.B., Stamatovic S.M., Keep R.F., Andjelkovic A.V.: Effects of the chemokine CCL2 on blood-brain barrier permeability during ischemia-reperfusion injury. J. Cereb. Blood Flow Metab. 2006; 26: 797–810.
  • 34. Dimitrijevic O.B., Stamatovic S.M., Keep R.F., Andjelkovic A.V.: Absence of the chemokine receptor CCR2 protects against cerebral ischemia/reperfusion injury in mice. Stroke 2007; 38: 1345–1353.
  • 35. Schönemeier B., Schulz S., Hoellt V., Stumm R.: Enhanced expression of the CXCl12/SDF-1 chemokine receptor CXCR7 after cerebral ischemia in the rat brain. J. Neuroimmunol. 2008; 198: 39–45.
  • 36. Wang Y., Deng Y., Zhou G.Q.: SDF-1α/CXCR4-mediated migration of systemically transplanted bone marrow stromal cells towards ischemic brain lesion in a rat model. Brain Res. 2008; 1195: 104–112.
  • 37. Wang X., Li X., Schmidt D.B. i wsp.: Identification and molecular characterization of rat CXCR3: receptor expression and interferon-inducible protein-10 binding are increased in focal stroke. Mol. Pharmacol. 2000; 57: 1190–1198.
  • 38. Terao S., Yilmaz G., Stokes K.Y. i wsp.: Blood cell-derived RANTES mediates cerebral microvascular dysfunction, inflammation, and tissue injury after focal ischemia-reperfusion. Stroke 2008; 39: 2560–2570.
  • 39. Yamasaki Y., Matsuo Y., Zagorski J. i wsp.: New therapeutic possibility of blocking cytokine-induced neutrophil chemoattractant on transient ischemic brain damage in rats. Brain Res. 1997; 759: 103–111.
  • 40. Mizushima N., Ohsumi Y., Yoshimori T.: Autophagosome formation in mammalian cells. Cell Struct. Funct. 2002; 27: 421–429.
  • 41. Uchiyama Y., Shibata M., Koike M. i wsp.: Autophagy-physiology and pathophysiology. Histochem. Cell Biol. 2008; 129: 407–420.
  • 42. Alirezaei M., Kemball C.C., Whitton J.L.: Autophagy, inflammation and neurodegenerative disease. Eur. J. Neurosci. 2011; 33: 197–204.
  • 43. Komatsu M., Waguri S., Ueno T. i wsp.: Impairment of starvation- induced and constitutive autophagy in Atg7-deficient mice. J. Cell Biol. 2005; 169: 425–434.
  • 44. Kuma A., Hatano M., Matsui M. i wsp.: The role of autophagy during the early neonatal starvation period. Nature 2004; 432: 1032–1036.
  • 45. Cuervo A.M.: Autophagy: in sickness and in health. Trends Cell. Biol. 2004; 14: 70–77.
  • 46. Adhami F., Liao G., Morozov Y.M. i wsp.: Cerebral ischemia- hypoxia induces intravascular coagulation and autophagy. Am. J. Pathol. 2006; 169: 566–583.
  • 47. Zhu C., Wang X., Xu F. i wsp.: The influence of age on apoptotic and other mechanisms of cell death after cerebral hypoxia- ischemia. Cell Death Differ. 2005; 12: 162–176.
  • 48. Xue L., Fletcher G.C., Tolkovsky A.M.: Mitochondria are selectively eliminated from eukaryotic cells after blockade of caspases during apoptosis. Curr. Biol. 2001; 11: 361–365.
  • 49. Pan T., Kondo S., Zhu W. i wsp.: Neuroprotection of rapamycin in lactacystin-induced neurodegeneration via autophagy enhancement. Neurobiol. Dis. 2008; 32: 16–25.
  • 50. Malagelada C., Jin Z.H., Jackson-Lewis V. i wsp.: Rapamycin protects against neuron death in in vitro and in vivo models of Parkinson’s disease. J. Neurosci. 2010; 30: 1166–1175.
  • 51. Carloni S., Girelli S., Scopa C. i wsp.: Activation of autophagy and Akt/CREB signaling play an equivalent role in the neuroprotective effect of rapamycin in neonatal hypoxia- ischemia. Autophagy 2010; 6: 366–377.
  • 52. Sheng R., Zhang L.S., Han R. i wsp.: Autophagy activation is associated with neuroprotection in a rat model of focal cerebral ischemic preconditioning. Autophagy 2010; 6: 482–494.
  • 53. Adhami F., Schloemer A., Kuan C.Y.: The roles of autophagy in cerebral ischemia. Autophagy 2007; 3: 42–44.
  • 54. Dennis P.B., Jaeschke A., Saitoh M. i wsp.: Mammalian TOR: a homeostatic ATP sensor. Science 2001; 294: 1102–1105.
  • 55. Codogno P., Meijer A.J.: Autophagy and signaling: their role in cell survival and cell death. Cell Death Differ. 2005; 12: 1509–1518.
  • 56. Semenza G.L.: Mitochondrial autophagy: life and breath of the cell. Autophagy 2008; 4: 534–536.
  • 57. Trapp B.D., Bö L., Mörk S., Chang A.: Pathogenesis of tissue injury in MS lesions. J. Neuroimmunol. 1999; 98: 49–56.
  • 58. Justicia C., Ramos-Cabrer P., Hoehn M.: MRI detection of secondary damage after stroke: chronic iron accumulation in the thalamus of the rat brain. Stroke 2008; 39: 1541–1547.
  • 59. Stys P.K.: General mechanisms of axonal damage and its prevention. J. Neurol. Sci. 2005; 233: 3–13.
  • 60. Lappe-Siefke C., Goebbels S., Gravel M. i wsp.: Disruption of Cnp1 uncouples oligodendroglial functions in axonal support and myelination. Nat. Genet. 2003; 33: 366–374.
  • 61. Taylor C.P.: Na+ currents that fail to inactivate. Trends Neurosci. 1993; 16: 455–460.
  • 62. Stys P.K.: Axonal degeneration in multiple sclerosis: is it time for neuroprotective strategies? Ann. Neurol. 2004; 55: 601–603.
  • 63. Stys P.K., Sontheimer H., Ransom B.R., Waxman S.G.: Noninactivating, tetrodotoxin-sensitive Na+ conductance in rat optic nerve axons. Proc. Natl Acad. Sci. USA 1993; 90: 6976–6980.
Document Type
article
Publication order reference
YADDA identifier
bwmeta1.element.psjd-803de345-6aa9-42ea-bc9c-4f3e4408d887
Identifiers
JavaScript is turned off in your web browser. Turn it on to take full advantage of this site, then refresh the page.