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Tahamtan, Mahshid, Shamsizadeh, Ali, Allahtavakoli, Mohammad, Nami, Mohammad, Mohammadi, Neda, Hassanshahi, Gholamhossein. (1396). Differential Expression of CXCL1, CXCL10, and CXCL12 in Response to Cerebral Ischemic Postconditioning in Rat Brain. سامانه مدیریت نشریات علمی, 3(4), 197-204. doi: 10.32598/jamsat.3.4.197
Mahshid Tahamtan; Ali Shamsizadeh; Mohammad Allahtavakoli; Mohammad Nami; Neda Mohammadi; Gholamhossein Hassanshahi. "Differential Expression of CXCL1, CXCL10, and CXCL12 in Response to Cerebral Ischemic Postconditioning in Rat Brain". سامانه مدیریت نشریات علمی, 3, 4, 1396, 197-204. doi: 10.32598/jamsat.3.4.197
Tahamtan, Mahshid, Shamsizadeh, Ali, Allahtavakoli, Mohammad, Nami, Mohammad, Mohammadi, Neda, Hassanshahi, Gholamhossein. (1396). 'Differential Expression of CXCL1, CXCL10, and CXCL12 in Response to Cerebral Ischemic Postconditioning in Rat Brain', سامانه مدیریت نشریات علمی, 3(4), pp. 197-204. doi: 10.32598/jamsat.3.4.197
Tahamtan, Mahshid, Shamsizadeh, Ali, Allahtavakoli, Mohammad, Nami, Mohammad, Mohammadi, Neda, Hassanshahi, Gholamhossein. Differential Expression of CXCL1, CXCL10, and CXCL12 in Response to Cerebral Ischemic Postconditioning in Rat Brain. سامانه مدیریت نشریات علمی, 1396; 3(4): 197-204. doi: 10.32598/jamsat.3.4.197

Differential Expression of CXCL1, CXCL10, and CXCL12 in Response to Cerebral Ischemic Postconditioning in Rat Brain

Journal of Advanced Medical Sciences and Applied Technologies
مقاله 3، دوره 3، شماره 4، اسفند 2017، صفحه 197-204    اصل مقاله (873.33 K)
نوع مقاله: Original Articles
شناسه دیجیتال (DOI): 10.32598/jamsat.3.4.197
نویسندگان
Mahshid Tahamtan1؛ Ali Shamsizadeh1؛ Mohammad Allahtavakoli1؛ Mohammad Nami2؛ Neda Mohammadi2؛ Gholamhossein Hassanshahi* 3
1Physiology Pharmacology Research Center, Rafsanjan University of Medical Sciences, Rafsanjan, Iran.
2Department of Neuroscience, School of Advanced Medical Sciences and Technologies, Shiraz University of Medical Sciences, Shiraz, Iran.
3Molecular Medicine Research Center, Rafsanjan University of Medical Sciences, Rafsanjan, Iran.
چکیده
Objectives: Cerebral ischemic preconditioning lessens stroke-induced injuries, but it is clinically feasible only when the occurrence of stroke is predictable. Reperfusion plays a critical role against cerebral injury after stroke; we tested the hypothesis that interrupting ischemia during early reperfusion, i.e. Postconditioning (POCO) affects CXC chemokine expression and further reduce inflammation in rat model of ischemia/reperfusion. Materials & Methods: Adult male Wistar rats (250-300 g) were used in this experiment. Using 4-vessel occlusion method, global cerebral ischemia was induced and POCO was performed by applying 3 cycles of 15-s/15-s reperfusion/reocclusion after a 45-s reperfusion (POCO-45-15/15). Western blotting analysis was used to investigate CXCL1, CXCL10 and CXCL12 expression 24 h, 48 h and one week after ischemic postconditioning (iPOCO).Results: Based on the results, iPOCO attenuates the expression of inflammatory chemokines CXCL1 and CXCL10 in hippocampus area of postconditioned rats, while the CXCL12 was not affected by iPOCO.Conclusion: Current findings may support chemokines role in iPOCO via reduction of inflammation. Also there could be a link between postconditioning, stress and inflammation through chemokines.
کلیدواژه‌ها
Chemokine؛ Global cerebral ischemia؛ Postconditioning
مراجع
  1. Koroshetz WJ, Moskowitz MA. Emerging treatments for stroke in humans. Trends in Pharmacological Sciences. 1996; 17(6):227–33. [DOI:10.1016/0165-6147(96)10020-1]
  2. Yang XM, Proctor JB, Cui L, Krieg T, Downey JM, Cohen MV. Multiple, brief coronary occlusions during early reperfusion protect rabbit hearts by targeting cell signaling pathways. Journal of the American College of Cardiology. 2004; 44(5):1103–10. [DOI:10.1016/j.jacc.2004.05.060]
  3. Zhao ZQ, Corvera JS, Halkos ME, Kerendi F, Wang NP, Guyton RA, et al. Inhibition of myocardial injury by ischemic postconditioning during reperfusion: Comparison with ischemic preconditioning. American Journal of Physiology-Heart and Circulatory Physiology. 2003; 285(2):H579-H88. [DOI:10.1152/ajpheart.01064.2002] [PMID]
  4. Burda J, Danielisova V, Nemethova M, Gottlieb M, Matiašova M, Domorakova I, et al. Delayed postconditionig initiates additive mechanism necessary for survival of selectively vulnerable neurons after transient ischemia in rat brain. Cellular and Molecular Neurobiology. 2006; 26(7-8):1141-51. [DOI:10.1007/s10571-006-9036-x] [PMID]
  5. Danielisova V, Nemethova M, Gottlieb M, Burda J. The changes in endogenous antioxidant enzyme activity after postconditioning. Cellular and Molecular Neurobiology. 2006; 26(7):1179-89. [DOI:10.1007/s10571-006-9034-z] [PMID]
  6. Zhao H, Sapolsky RM, Steinberg GK. Interrupting reperfusion as a stroke therapy: Ischemic postconditioning reduces infarct size after focal ischemia in rats. Journal of Cerebral Blood Flow & Metabolism. 2006; 26(9):1114–21. [DOI:10.1038/sj.jcbfm.9600348]
  7. Jiang X, Shi E, Nakajima Y, Sato S. Postconditioning, a series of brief interruptions of early reperfusion, prevents neurologic injury after spinal cord ischemia. Annals of Surgery. 2006; 244(1):148–53. [DOI:10.1097/01.sla.0000217608.08582.35]
  8. Rehni AK, Singh N. Role of phosphoinositide 3-kinase in ischemic postconditioning-induced attenuation of cerebral ischemia-evoked behavioral deficits in mice. Pharmacological Reports. 2007; 59(2):192-8. [PMID]
  9. Zhang F, Hu EC, Gerzenshtein J, Lei MP, Lineaweaver WC. The expression of proinflammatory cytokines in the rat muscle flap with ischemia-reperfusion injury. Annals of Plastic Surgery. 2005; 54(3):313-7.
  10. Ahmadi Z, Arababadi MK, Hassanshahi G. CXCL10 activities, biological structure, and source along with its significant role played in pathophysiology of type I diabetes mellitus. Inflammation. 2013; 36(2):364-71. [DOI:10.1007/s10753-012-9555-1] [PMID]
  11. Hassanshahi G, Jafarzadeh A, Ghorashi Z, Sheikholeslami NZ, Dickson AJ. Expression of IP-10 chemokine is regulated by pro-inflammatory cytokines in cultured hepatocytes. Iranian Journal of Allergy, Asthma and Immunology. 2007; 6(3):115-22.
  12. Asiabanha M, Asadikaram G, Rahnema A, Mahmoodi M, Hasanshahi G, Hashemi M, et al. Chronic opium treatment can differentially induce brain and liver cells apoptosis in diabetic and non-diabetic male and female rats. The Korean Journal of Physiology and Pharmacology. 2011; 15(6):327-32. [DOI:10.4196/kjpp.2011.15.6.327]
  13. Pulsinelli WA, Brierley JB. A new model of bilateral hemispheric ischemia in the unanesthetized rat. Stroke. 1979; 10(3):267-72. [DOI:10.1161/01.STR.10.3.267]
  14. Wang JY, Shen J, Gao Q, Ye ZG, Yang SY, Liang HW, et al. Ischemic postconditioning protects against global cerebral ischemia/reperfusion-induced injury in rats. Stroke. 2008; 39(3):983-90. [DOI:10.1161/STROKEAHA.107.499079] [PMID]
  15. Zhang W, Miao Y, Zhou S, Wang B, Luo Q, Qiu Y. Involvement of glutamate transporter-1 in neuroprotection against global brain ischemia-reperfusion injury induced by postconditioning in rats. International Journal of Molecular Sciences. 2010; 11(11):4407. [DOI:10.3390/ijms11114407]
  16. Luangsay S, Wittamer V, Bondue B, De Henau O, Rouger L, Brait M, et al. Mouse chemR23 is expressed in dendritic cell subsets and macrophages, and mediates an anti-inflammatory activity of chemerin in a lung disease model. The Journal of Immunology. 2009; 183(10):6489-99. [DOI:10.4049/jimmunol.0901037] [PMID]
  17. Duilio C, Ambrosio G, Kuppusamy P, DiPaula A, Becker LC, Zweier JL. Neutrophils are primary source of O2radicals during reperfusion after prolonged myocardial ischemia. American Journal of Physiology-Heart and Circulatory Physiology. 2001; 280(6):H2649-H57. [DOI:10.1152/ajpheart.2001.280.6.H2649] [PMID]
  18. Jeroudi MO, Hartley CJ, Bolli R. Myocardial reperfusion injury: Role of oxygen radicals and potential therapy with antioxidants. American Journal of Cardiology. 1994; 73(6):B2-B7. [DOI:10.1016/0002-9149(94)90257-7]
  19. Kevin LG, Camara AKS, Riess ML, Novalija E, Stowe DF. Ischemic preconditioning alters real-time measure of O2 radicals in intact hearts with ischemia and reperfusion. American Journal of Physiology-Heart and Circulatory Physiology. 2003; 284(2):H566-H74. [DOI:10.1152/ajpheart.00711.2002] [PMID]
  20. Fan H, Sun B, Gu Q, Lafond-Walker A, Cao S, Becker LC. Oxygen radicals trigger activation of NF-kappaB and AP-1 and upregulation of ICAM-1 in reperfused canine heart. American journal of physiology Heart and circulatory physiology. 2002; 282(5):H1778-86. [DOI:10.1152/ajpheart.00796.2000] [PMID]
  21. Hassanshahi G, Jafarzadeh A, Dickson AJ. Expression of stromal derived factor alpha (SDF-1α) by primary hepatocytes following isolation and heat shock stimulation. Iranian Journal of Allergy, Asthma and Immunology. 2008; 7(2):61-8.
  22. Albertine KH, Weyrich AS, Ma XL, Lefer DJ, Becker LC, Lefer AM. Quantification of neutrophil migration following myocardial ischemia and reperfusion in cats and dogs. Journal of Leukocyte Biology. 1994; 55(5):557-66. [DOI:10.1002/jlb.55.5.557]
  23. Dreyer WJ, Michael LH, West MS, Smith CW, Rothlein R, Rossen RD, et al. Neutrophil accumulation in ischemic canine myocardium. Insights into time course, distribution, and mechanism of localization during early reperfusion. Circulation. 1991; 84(1):400-11. [DOI:10.1161/01.CIR.84.1.400] [PMID]
  24. Chatelain P, Latour JG, Tran D, de Lorgeril M, Dupras G, Bourassa M. Neutrophil accumulation in experimental myocardial infarcts: Relation with extent of injury and effect of reperfusion. Circulation. 1987; 75(5):1083-90. [DOI:10.1161/01.CIR.75.5.1083] [PMID]
  25. Mehta JL, Nichols WW, Mehta P. Neutrophils as potential participants in acute myocardial ischemia: Relevance to reperfusion. Journal of the American College of Cardiology. 1988; 11(6):1309-16. [DOI:10.1016/0735-1097(88)90297-5]
  26. Tsao PS, Aoki N, Lefer DJ, Johnson G, Lefer AM. Time course of endothelial dysfunction and myocardial injury during myocardial ischemia and reperfusion in the cat. Circulation. 1990; 82(4):1402-12. [DOI:10.1161/01.CIR.82.4.1402] [PMID]
  27. Zhao ZQ, Nakamura M, Wang NP, Velez DA, Hewan-Lowe KO, Guyton RA, et al. Dynamic progression of contractile and endothelial dysfunction and infarct extension in the late phase of reperfusion. Journal of Surgical Research. 2000; 94(2):133-44. [DOI:10.1006/jsre.2000.6029] [PMID]
  28. Curtis WE, Gillinov AM, Wilson IC, Bator JM, Burch RM, Cameron DE, et al. Inhibition of neutrophil adhesion reduces myocardial infarct size. The Annals of Thoracic Surgery. 1993; 56(5):1069-73. [DOI:10.1016/0003-4975(95)90015-2]
  29. Forman MB, Virmani R, Puett DW. Mechanisms and therapy of myocardial reperfusion injury. Circulation. 1990; 81(3 Suppl):IV69-78. [PMID]
  30. Hartman JC, Anderson DC, Wiltse AL, Lane CL, Rosenbloom CL, Manning AM, et al. Protection of ischemic/reperfused canine myocardium by CL18/6, a monoclonal antibody to adhesion molecule ICAM-1. Cardiovascular Research. 1995; 30(1):47-54. [DOI:10.1016/0008-6363(95)00015-1]
  31. Baxter GF. The neutrophil as a mediator of myocardial ischemia-reperfusion injury: Time to move on. Basic Research in Cardiology. 2002; 97(4):268-75. [DOI:10.1007/s00395-002-0366-7] [PMID]
  32. Bergin PF, Doppelt JD, Kephart CJ, Benke MT, Graeter JH, Holmes AS, et al. Comparison of minimally invasive direct anterior versus posterior total hip arthroplasty based on inflammation and muscle damage markers. The Journal of Bone and Joint Surgery-American Volume. 2011; 93(15):1392–8. [DOI:10.2106/jbjs.j.00557]
  33. Tüzün E, Li J, Wanasen N, Soong L, Christadoss P. Immunization of mice with T cell-dependent antigens promotes IL-6 and TNF-α production in muscle cells. Cytokine. 2006; 35(1-2):100–6. [DOI:10.1016/j.cyto.2006.05.009]
  34. Park JW, Ma SN, Song ES, Song CH, Chae MR, Park BH, et al. Pulmonary damage by Vibrio vulnificus cytolysin. Infection and Immunity. 1996; 64(7):2873-6. [PMID] [PMCID]
  35. Fan C, Zwacka RM, Engelhardt JF. Therapeutic approaches for ischemia/reperfusion injury in the liver. Journal of Molecular Medicine. 1999; 77(8):577-92. [DOI:10.1007/s001099900029] [PMID]
  36. Tsung A, Kaizu T, Nakao A, Shao L, Bucher B, Fink MP, et al. Ethyl pyruvate ameliorates liver ischemia-reperfusion injury by decreasing hepatic necrosis and apoptosis. Transplantation. 2005; 79(2):196–204. [DOI:10.1097/01.tp.0000151681.07474.2e]
  37. Packard AE, Leung PY, Vartanian KB, Stevens SL, Bahjat FR, Stenzel-Poore MP. TLR9 bone marrow chimeric mice define a role for cerebral TNF in neuroprotection induced by CpG preconditioning. Journal of Cerebral Blood Flow & Metabolism. 2012; 32(12):2193–200. [DOI:10.1038/jcbfm.2012.140]
  38. Sakata H, Narasimhan P, Niizuma K, Maier CM, Wakai T, Chan PH. Interleukin 6-preconditioned neural stem cells reduce ischaemic injury in stroke mice. Brain. 2012; 135(11):3298-310. [DOI:10.1093/brain/aws259] [PMID] [PMCID]
  39. Masayuki K, Tao Sheng L, Takahiro K, Mako O, Shu Lan Q, Kimikazu H. Increased expression of CXCR4 and integrin αM in hypoxia‐preconditioned cells contributes to improved cell retention and angiogenic potency. Journal of Cellular Physiology. 2009; 220(2):508-14. [DOI:10.1002/jcp.21803] [PMID]
  40. Tang YL, Zhu W, Cheng M, Chen L, Zhang J, Sun T, et al. Hypoxic preconditioning enhances the benefit of cardiac progenitor cell therapy for treatment of myocardial infarction by inducing CXCR4 expression. Circulation Research. 2009; 104(10):1209-16. [DOI:10.1161/CIRCRESAHA.109.197723] [PMID] [PMCID]
  41. Voigtsberger MDS, Lachmann MDPDRobert A, Leutert MDAnik C, Schläpfer MDM, Booy C, Reyes L, et al. Sevoflurane ameliorates gas exchange and attenuates lung damage in experimental lipopolysaccharide-induced lung injury. Anesthesiology. 2009; 111(6):1238-48. [DOI:10.1097/ALN.0b013e3181bdf857] [PMID]
  42. Janabi N, Hau I, Tardieu M. Negative feedback between prostaglandin and α- and β-Chemokine synthesis in human microglial cells and astrocytes. The Journal of Immunology. 1999; 162(3):1701-6. [PMID]
  43. Patrizia S, Carlo L, Cristina P, Paola A, Alberto M, Silvano S, et al. Neutrophils produce biologically active macrophage inflammatory protein‐3α (MIP‐3α) / CCL20 and MIP‐3β / CCL19. European Journal of Immunology. 2001; 31(7):1981-8. [DOI:10.1002/1521-4141(200107)31:73.0.CO; 2-X]
  44. Liu T, Young PR, McDonnell PC, White RF, Barone FC, Feuerstein GZ. Cytokine-induced neutrophil chemoattractant mRNA expressed in cerebral ischemia. Neuroscience Letters. 1993; 164(1-2):125–8. [DOI:10.1016/0304-3940(93)90873-j]
  45. Yamasaki Y, Matsuo Y, Matsuura N, Onodera H, Itoyama Y, Kogure K. Transient increase of cytokine-induced neutrophil chemoattractant, a member of the interleukin-8 family, in ischemic brain areas after focal ischemia in rats. Stroke. 1995; 26(2):318-23. [DOI:10.1161/01.STR.26.2.318] [PMID]
  46. Becker KJ. Inflammation and acute stroke. Current Opinion in Neurology. 1998; 11(1):45-9. [DOI:10.1097/00019052-199802000-00008] [PMID]
  47. Kostulas N, Kivisäkk P, Huang Y, Matusevicius D, Kostulas V, Link H. Ischemic stroke is associated with a systemic increase of blood mononuclear cells expressing interleukin-8 mRNA. Stroke. 1998; 29(2):462-6. [DOI:10.1161/01.STR.29.2.462] [PMID]
  48. Kostulas N, Pelidou SH, Kivisäkk P, Kostulas V, Link H. Increased IL-1β, IL-8, and IL-17 mRNA expression in blood mononuclear cells observed in a prospective ischemic stroke study. Stroke. 1999; 30(10):2174-9. [DOI:10.1161/01.STR.30.10.2174] [PMID]
  49. Tarkowski E, Rosengren L, Blomstrand C, Wikkelsö C, Jensen C, Ekholm S, et al. Intrathecal release of pro-and anti-inflammatory cytokines during stroke. Clinical & Experimental Immunology. 1997; 110(3):492-9. [DOI:10.1046/j.1365-2249.1997.4621483.x] [PMCID]
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