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【文摘发布】Lipocalin-2对移植心缺血再灌注损伤炎
Author:F. Aigner, H. T. Maier，H. G. Schwelberger，et al.
Resource：American Journal of Transplantation，Volume 7 Issue 4 Page 779 - April 2007 http://www.blackwell-synergy.com/doi/abs/10.1111/j.1600-6143.2006.01723.x
Impact Factor：6.002
Abstract:
Ischemia and reperfusion (IR) are known to negatively affect early allograft function following solid organ transplantation. Lipocalin-2 (Lcn-2) has been described as a marker and potential positive modulator of acute inflammation during these processes. Using a heterotopic murine heart transplant model we previously found that IR resulted in a pronounced upregulation of Lcn-2 mRNA in the heart at 12 (22.7-fold increase) and 24 h (9.8-fold increase) of reperfusion. We now confirm this increase at the protein level and provide evidence for infiltrating polymorphonuclear cells as the primary source of Lcn-2 protein. Lcn-2 levels are increased 6.6-fold at 12 h, 11.4-fold at 24 h and 6.4 fold at 48 h after reperfusion. In Lcn-2－/－ grafts the number of infiltrating granulocytes is reduced by 54% (p < 0.05) at 2 h, 79% (p < 0.01) at 12 h, 72% (p < 0.01) at 24 h and 52% (p < 0.01) at 48 h after reperfusion compared to Lcn-2+/+ grafts, without any differences in cardiomyocyte apoptosis. These data suggest a function of Lcn-2 in the initiation of the inflammatory response. Moreover, an increase in Lcn-2 is not only restricted to the transplanted heart, but is also observed in the kidney, hinting at a possible involvement of Lcn-2 in the systemic response to IR.
缺血再灌注损伤对于器官移植的意义是不言而喻的，也是科研课题设计的热点，本文给出新的靶点。 本人已认领该文编译，48小时后若未提交译文，请其他战友自由认领。 Title：Lipocalin-2 Regulates the Inflammatory Response During Ischemia and Reperfusion of the Transplanted Heart.
标题：Lipocalin-2对移植心缺血再灌注损伤炎症反应的调节
Author:F. Aigner, H. T. Maier，H. G. Schwelberger，et al.
作者：F. Aigner, H. T. Maier，H. G. Schwelberger等
Resource：American Journal of Transplantation，Volume 7 Issue 4 Page 779 - April 2007
文章来源：美国移植杂志，第7卷第4期，779.2007年4月.
Impact Factor：6.002
影响因子：6.002
Abstract:
摘要：
Ischemia and reperfusion (IR) are known to negatively affect early allograft function following solid organ transplantation.
在实体器官移植后，缺血再灌注对早期移植物功能有不良影响。
Lipocalin-2 (Lcn-2) has been described as a marker and potential positive modulator of acute inflammation during these processes.
在这些过程中，Lipocalin-2 (Lcn-2)被认为是急性炎症反应的一种标记及潜在的阳性调节因子。
Using a heterotopic murine heart transplant model we previously found that IR resulted in a pronounced upregulation of Lcn-2 mRNA in the heart at 12 (22.7-fold increase) and 24 h (9.8-fold increase) of reperfusion.
我们先前通过大鼠异位心脏移植模型发现，缺血再灌注会导致心脏的Lcn-2 mRNA于再灌注12h（增加22.7倍）和24h（增加9.8倍）有明显增量调节。
We now confirm this increase at the protein level and provide evidence for infiltrating polymorphonuclear cells as the primary source of Lcn-2 protein.
现在我们可以确定这种蛋白水平的增加并能提供浸润多形核细胞为Lcn-2蛋白原始来源的证据。
Lcn-2 levels are increased 6.6-fold at 12 h, 11.4-fold at 24 h and 6.4 fold at 48 h after reperfusion.
Lcn-2水平于再灌注12h增加6.6倍，24h增加11.4倍，48h增加6.4倍。
In Lcn-2/ grafts the number of infiltrating granulocytes is reduced by 54% (p < 0.05) at 2 h, 79% (p < 0.01) at 12 h, 72% (p < 0.01) at 24 h and 52% (p < 0.01) at 48 h after reperfusion compared to Lcn-2+/+ grafts, without any differences in cardiomyocyte apoptosis.
与Lcn-2+/+ 移植物相比，在Lcn-2-/-移植物中，浸润粒细胞的数目于再灌注2 h减少54%(p < 0.05)，12 h 减少79% (p < 0.01)，24 h 减少72% (p < 0.01)，48 h 减少52% (p < 0.01)，在心肌细胞凋亡方面没有任何差别。
These data suggest a function of Lcn-2 in the initiation of the inflammatory response.
这些数据说明，Lcn-2在炎症应答开始中的作用。
Moreover, an increase in Lcn-2 is not only restricted to the transplanted heart, but is also observed in the kidney, hinting at a possible involvement of Lcn-2 in the systemic response to IR.
另外，Lcn-2增加不仅仅局限于移植的心脏，在肾脏中也可见，这暗示在缺血再灌注的全身应答中可能与Lcn-2有关。 编译：（中文字符：337）
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作者:admin@医学,生命科学 2011-07-27 05:36
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