TNF-α调节局部脑缺血区ICAM-1 mRNA的表达
作者：刘勇 雷万龙 袁群芳 姚志彬
单位：刘勇(西安医科大学解剖教研室)；雷万龙 袁群芳 姚志彬(中山医科大学解剖教研室，广州 510089)
关键词：脑缺血/再灌流；ICAM-1 mRNA；TNF-
解剖科学进展000314摘 要：目的，为了证实TNF-α对局部脑缺血/再灌流区ICAM-1 mRNA表达的影响；方法：运用原位杂交技术对60只雄性SD大鼠进行了研究。结果：局部脑缺血/再灌流诱导脑微血管和毛细血管以及局部炎症细胞ICAM-1 mRNA的表达，其表达发生于脑缺血1h/再灌流2h，再灌流8h达到高峰。TNF-α明显的加强脑缺血区ICAM-1 mRNA的表达，其作用在脑缺血1h/再灌流2h至8h均较明显。再灌流4h，TNF-α的诱导作用最显著。结论：局部脑缺血/再灌流诱导ICAM-1 mRNA表达，TNF-α对其表达具有明显的促进作用。提示TNF-α通过调节ICAM-1 mRNA的表达参与脑缺血/再灌流损伤病理过程。 TNF-α Upregulates ICAM-1 mRNA Expression in Focal Cerebral lschemic Area in Rats
, http://www.100md.com
Lei Wanlong
(Department of Anatomy, Sun Yat-sen University of Medical Sciences, Guangzhou 510089)
Liu Yong
(Department of Anatomy, Xi’an Medical University, Xi’an)
Yuan Ounfang
(Department of Anatomy, Sun Yat-sen University of Medical Sciences, Guangzhou 510089)
Abstract：Objective:To test the effect of TNF-α on ICAM-1 mRNA expression in ischemic at rat. Method: In situ hybridization histochemistry was used in the study. Results: ① Focal ischemia/reperfusion-induced ICAM-1 mRNA expression occurred on the microvascular and capillary endothelial cells, and focal inflammatory cells at lh ischemia/2h reperfusion, peaked at 8h reperfusion. ② TNF-α induced strongly ICAM-1 mRNA expression in the ischemic cerebral area during 2h-8h reperfusion, and the strongest induce-effect was at the time point of 4h reperfusion. Conclusion: Focal cerebral ischemia/reperfusion induced ICAM-1 mRNA expression in the ischemic brain, and TNF-α accelerated ICAM-1 mRNA expression. This result indicated that TNF-α participated in the pathogenesis of ischemic cerebral injury.
, http://www.100md.com
Keywords：cerebral ischemia/reperfusion; ICAM-1; TNF-α
参考文献：
[1]Lindsberg J, Carpen O, Paetau A, et al. Endothelial ICAM-1 expression associated with inflammatory cell response in human ischemic stroke. Circulation, 1996, 94: 939
[2]Zhang RL, Chopp M, Jiang N, et al. Anti-intercellular adhesion molecule-1 antibody reduces ischemic cell damage after transient but not permanent middle cerebral artery occlusion in the wistar rat. Stroke, 1995, 26: 1438
, http://www.100md.com
[3]Zhang RL, Chopp M, Zaloga C, et al. The temporal profiles of ICAM-1 protein and mRNA expression after transient MCA occlusion in the rat. Brain Res, 1995, 682: 182
[4]Lin T, clark PK, McDonnell PC, et al. Tumor necrosis factor-α expression in ischemic neurons. Stroke, 1994, 25: 1481
[5]Barone FC, Arvin B, White RF, et al. Tumor necrosis factor-α, a mediator of focal ischemic brain injury. Stroke, 1994, 25: 1481
, 百拇医药
[6]Zund G, Dzus AL, McGuirk DK, et al. Hypoxic stress alone does not modulate endothelial surface expression of bovine Eelectin and intercellular dhesion molecule-(ICAM-1). Swiss Surg Suppl, 1996, 1: 41
[7]Barone FC, Schmidt DB, Hillegass LM, et al. Reperfusion increases neutrophils and leukotriene B4 receptor binding in rat focal ischemia. Strike, 1992, 23: 1337
[8]Wang X, Feuerstein GZ. Induced expression of adhesion molecules following focal brain ischemia. J Neurotrauma, 1995, 12: 825
, 百拇医药
[9]Eppihimer MJ, Granger DN. Ischemia/reperfusion-induced leukocyte-endothelial interactions in post capillary venules. Stroke, 1997, 8: 16
[10]Hurwitz AA, Lyman WD, Guida MP, et al. Tumor necrosis factor α induces adhesion molecule expression on human fetal astrocytes. J Exp Med, 1992, 176: 1631
[11]Wyble CW, Desai TR, Clark ET, et al. Physiologic concentrations of TNF alpha and IL-1 beta released from reperfused human intestine upregulate E-selectin and ICAM-1. J Surg Res, 1996, 63: 333
, 百拇医药
[12]Frangoginnis NG, Lindsey ML, Michael LH, et al. Resident cardiac mast cells degranulate and release preformed TNF-alpha, initiatin the cytokine cascade in experimental canine myocardial ischemia/reperfusion. Circulation, 1998, 98: 699
[13]Colletti LM, Cortis A, Lukacs N, et al. Tumor necrosis factor upregulates intercellular adhesion molecule 1, which is important in the neutrophil-dependent lung and liver injury associated with hepatic isehemia and reperfusion in the rat. Shock, 1998, 10: 182
, 百拇医药
[14]Stanimirovic DB, Wong J, Shapiro A, et al. Increase in surface expression of ICAM-1, VCAM-1 and E-seleetin in human cerebromicrovaseular endotheilial cells subjected to ischemialike indults. Acta Neuroehir Suppl Wien, 1997, 70: 12
[15]Wuthrich RP. Tumor necrosis faetor-a and interleukin-1 stimulated intercellular adhesion molecule-1 expression by murine tubular epithelial cells is transeriptionnally regulated and involves protein kinase C. Renal Physiol Biochem, 1992, 15: 302
[16]Read MA, Neish AS, Luscinskas FW, et al. The proteasome pathway is required for cytokineinduced endothelial leukocyte adhesion molecule expression. Immunity, 1995, 2: 493
[17]Clemens JA, Stephenson DT, Smalstig EB, et al. Global ischemia activates nuclear factor-кB in forebrain neurons of rats. Stroke, 1997, 28: 1073, 百拇医药
单位：刘勇(西安医科大学解剖教研室)；雷万龙 袁群芳 姚志彬(中山医科大学解剖教研室，广州 510089)
关键词：脑缺血/再灌流；ICAM-1 mRNA；TNF-
解剖科学进展000314摘 要：目的，为了证实TNF-α对局部脑缺血/再灌流区ICAM-1 mRNA表达的影响；方法：运用原位杂交技术对60只雄性SD大鼠进行了研究。结果：局部脑缺血/再灌流诱导脑微血管和毛细血管以及局部炎症细胞ICAM-1 mRNA的表达，其表达发生于脑缺血1h/再灌流2h，再灌流8h达到高峰。TNF-α明显的加强脑缺血区ICAM-1 mRNA的表达，其作用在脑缺血1h/再灌流2h至8h均较明显。再灌流4h，TNF-α的诱导作用最显著。结论：局部脑缺血/再灌流诱导ICAM-1 mRNA表达，TNF-α对其表达具有明显的促进作用。提示TNF-α通过调节ICAM-1 mRNA的表达参与脑缺血/再灌流损伤病理过程。 TNF-α Upregulates ICAM-1 mRNA Expression in Focal Cerebral lschemic Area in Rats
, http://www.100md.com
Lei Wanlong
(Department of Anatomy, Sun Yat-sen University of Medical Sciences, Guangzhou 510089)
Liu Yong
(Department of Anatomy, Xi’an Medical University, Xi’an)
Yuan Ounfang
(Department of Anatomy, Sun Yat-sen University of Medical Sciences, Guangzhou 510089)
Abstract：Objective:To test the effect of TNF-α on ICAM-1 mRNA expression in ischemic at rat. Method: In situ hybridization histochemistry was used in the study. Results: ① Focal ischemia/reperfusion-induced ICAM-1 mRNA expression occurred on the microvascular and capillary endothelial cells, and focal inflammatory cells at lh ischemia/2h reperfusion, peaked at 8h reperfusion. ② TNF-α induced strongly ICAM-1 mRNA expression in the ischemic cerebral area during 2h-8h reperfusion, and the strongest induce-effect was at the time point of 4h reperfusion. Conclusion: Focal cerebral ischemia/reperfusion induced ICAM-1 mRNA expression in the ischemic brain, and TNF-α accelerated ICAM-1 mRNA expression. This result indicated that TNF-α participated in the pathogenesis of ischemic cerebral injury.
, http://www.100md.com
Keywords：cerebral ischemia/reperfusion; ICAM-1; TNF-α
参考文献：
[1]Lindsberg J, Carpen O, Paetau A, et al. Endothelial ICAM-1 expression associated with inflammatory cell response in human ischemic stroke. Circulation, 1996, 94: 939
[2]Zhang RL, Chopp M, Jiang N, et al. Anti-intercellular adhesion molecule-1 antibody reduces ischemic cell damage after transient but not permanent middle cerebral artery occlusion in the wistar rat. Stroke, 1995, 26: 1438
, http://www.100md.com
[3]Zhang RL, Chopp M, Zaloga C, et al. The temporal profiles of ICAM-1 protein and mRNA expression after transient MCA occlusion in the rat. Brain Res, 1995, 682: 182
[4]Lin T, clark PK, McDonnell PC, et al. Tumor necrosis factor-α expression in ischemic neurons. Stroke, 1994, 25: 1481
[5]Barone FC, Arvin B, White RF, et al. Tumor necrosis factor-α, a mediator of focal ischemic brain injury. Stroke, 1994, 25: 1481
, 百拇医药
[6]Zund G, Dzus AL, McGuirk DK, et al. Hypoxic stress alone does not modulate endothelial surface expression of bovine Eelectin and intercellular dhesion molecule-(ICAM-1). Swiss Surg Suppl, 1996, 1: 41
[7]Barone FC, Schmidt DB, Hillegass LM, et al. Reperfusion increases neutrophils and leukotriene B4 receptor binding in rat focal ischemia. Strike, 1992, 23: 1337
[8]Wang X, Feuerstein GZ. Induced expression of adhesion molecules following focal brain ischemia. J Neurotrauma, 1995, 12: 825
, 百拇医药
[9]Eppihimer MJ, Granger DN. Ischemia/reperfusion-induced leukocyte-endothelial interactions in post capillary venules. Stroke, 1997, 8: 16
[10]Hurwitz AA, Lyman WD, Guida MP, et al. Tumor necrosis factor α induces adhesion molecule expression on human fetal astrocytes. J Exp Med, 1992, 176: 1631
[11]Wyble CW, Desai TR, Clark ET, et al. Physiologic concentrations of TNF alpha and IL-1 beta released from reperfused human intestine upregulate E-selectin and ICAM-1. J Surg Res, 1996, 63: 333
, 百拇医药
[12]Frangoginnis NG, Lindsey ML, Michael LH, et al. Resident cardiac mast cells degranulate and release preformed TNF-alpha, initiatin the cytokine cascade in experimental canine myocardial ischemia/reperfusion. Circulation, 1998, 98: 699
[13]Colletti LM, Cortis A, Lukacs N, et al. Tumor necrosis factor upregulates intercellular adhesion molecule 1, which is important in the neutrophil-dependent lung and liver injury associated with hepatic isehemia and reperfusion in the rat. Shock, 1998, 10: 182
, 百拇医药
[14]Stanimirovic DB, Wong J, Shapiro A, et al. Increase in surface expression of ICAM-1, VCAM-1 and E-seleetin in human cerebromicrovaseular endotheilial cells subjected to ischemialike indults. Acta Neuroehir Suppl Wien, 1997, 70: 12
[15]Wuthrich RP. Tumor necrosis faetor-a and interleukin-1 stimulated intercellular adhesion molecule-1 expression by murine tubular epithelial cells is transeriptionnally regulated and involves protein kinase C. Renal Physiol Biochem, 1992, 15: 302
[16]Read MA, Neish AS, Luscinskas FW, et al. The proteasome pathway is required for cytokineinduced endothelial leukocyte adhesion molecule expression. Immunity, 1995, 2: 493
[17]Clemens JA, Stephenson DT, Smalstig EB, et al. Global ischemia activates nuclear factor-кB in forebrain neurons of rats. Stroke, 1997, 28: 1073, 百拇医药