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抑制白细胞浸润对溶栓治疗细胞凋亡的影响

Effects of thrombolytic therapy combined with inhibition of leukocytes infiltration in a rat embolic stroke model
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摘要 目的观察Dextransulfate对白细胞浸润的抑制作用以及抑制白细胞浸润对溶栓治疗后细胞凋亡的影响。方法栓塞大鼠大脑中动脉后 30分钟 ,静脉给予Dextransulfate或生理盐水 ,缺血4小时经颈外动脉注入尿激酶溶栓治疗 ,缺血 12小时或 2 4小时 ,应用免疫组织化学方法观察缺血周边区白细胞浸润 ,TUNEL法检测细胞凋亡的变化。结果在缺血周边区 ,联合溶栓组浸润白细胞数较单纯溶栓组明显减少 (P <0 0 1) ;溶栓治疗后缺血周边区有大量的神经细胞凋亡 ;联合溶栓组凋亡细胞数较单纯溶栓组明显减少 (P <0 0 1)。结论Dextransulfate能明显抑制白细胞浸润 ,抑制白细胞浸润可以减少溶栓治疗后神经细胞凋亡。 Objective To study the effects of administration of urokinasecombined with dextran sulfate on leukocytes infiltration and apoptosis in a rat embolic stroke model. Methods Dextran sulfate (4mg/kg) or saline was intravenously administered after 30 min ischemia and urokinase (5000ц/kg) was injected through the catheter in ECA after 4hrs ischemia in rat embolic stroke model. At 12hrs or 24hrs after ischemia, leukocytes infiltration were evaluated by; munohistochemistry, apoptosis were detected by TUNEL. Results There were a plenty of apoptosis of neurons in margin of ischemia after thrombolysis. 24hrs of after ischemia, leukocytes infiltration as well as apoptosis of neurons were significantly reduced in treated with urokinase and dextran sulfate at 4hrs compared with those in treated with urokinase alone( P <0.01). Conclusion Combined with thrombolysis, dextran sulfate could significantly inhibit leukocytes infiltration and apoptosis of neurons.
出处 《贵州医药》 CAS 2002年第6期489-490,共2页 Guizhou Medical Journal
关键词 白细胞浸润 血栓栓塞 溶栓治疗 DEXTRAN SULFATE 白细胞 细胞凋亡 脑梗死 再灌注损伤 Thromboembolic stroke Thrombolytic therapy Dextran sulfate Leukocyte Apoptosis
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  • 1[1]Suzuki H,Abe K,Tojo SJ,et al. Reduction of ischemic brain injury by anti-P-selectin monoclonal antibody after permanent middle cerebral artery occlusion in rat. Neurol Res, 1999,21(3):269.
  • 2[2]Busch E,Kruger K,Hossmann KA.Improved model of thromboembolic stroke and rt-PA in the rat. Brain Res, 1997,788:16.
  • 3[3]Yang Y, Li Q, Miyashita H, et al. Usefulness of postischemicthrombolysis with or without neuroprotection in a focal embolicmodel of cerebral ischemia. J Neurosurg,2000,92:841.
  • 4[4]Connolly ES,Winfree CJ,Springer TA,et al. Cerebral protectionin homozygous null ICAM- 1 mice after middle cerebral artery occlusion role of neutrophil adhesion in the pathogenesis of stroke.J Clin Invest, 1996,97:209.
  • 5[5]Soriano SG, Lipton SA, Wang YF, et al. Intercellular adhesionmoleculo-1 deficient mice are less susceptible to cerebra ischemia-reperfusion injury. Ann Neurol, 1996,39:295.
  • 6[6]Zhang ZG,Chopp M,Tang WX,et al. Postischemic treatment ( 2-h) with anti-CD11b and anti-CD18 monoclonal antibodies areneuroprotective after transient (2h) focal cerebral ischemia inthe rat. Brain Res, 1995,698(1-2) :79.
  • 7[7]Peter K, Schwarz M, Conradt C, et al. Heparin inhibits ligandbinding to the leukocyte integrin Mac-1 (CD11b/CD18) .Circulation, 1999,100(14): 1533.
  • 8[8]YanakaK, Spellnan SR, McCarthy .JB, et al. Reduction of braininjury using heparin to inhibit leukocyte accumulation in a ratmodel of transient focal cerebral ischemia. 11 Dose-response effect and the the apeutic window. J Neurosurg, 1996,85:1108.
  • 9[9]Snider BJ,G ottron FJ, Choi DW,et al. Apoptosis and necrosis incerebrovascular disease. Ann N Y Acad Sci,1999,893:243.
  • 10[10]Chopp M,Li Y,Jiang N,et al. Antibodies against adhesion molecules reduce apoptosis after transient middle cerebral artery occlusion in rat brain. J Cereb Blood Flow Metab, 1996,16:578.

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