Effects of estrogen on leukocyte adhesion after transient forebrain ischemia.

Effects of estrogen on leukocyte adhesion after transient forebrain ischemia.
复制标题

雌激素对短暂前脑缺血后白细胞粘附的影响。

DOI:
10.1161/01.str.31.9.2231
复制
发表时间:
2000
期刊:
影响因子:
8.3
通讯作者:
Pelligrino,DA
Pelligrino,DA
中科院分区:
医学1区
文献类型:
--
作者:
Santizo,RA;Anderson,S;Ye,S;Koenig,HM;Pelligrino,DA

文献摘要

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背景和目的-最近的研究结果表明,雌激素(即17β-雌二醇[E2])在短暂性全脑和局灶性缺血模型中提供神经保护作用。增强的缺血后白细胞粘附和浸润与脑以及其他组织中的神经病理学有关。我们最近发现,雌激素减少白细胞粘附在脑循环中的雌性大鼠在静息conditions. Methods,我们比较了白细胞粘附在软脑膜小静脉在体内完整的,卵巢切除(OVX),和E2-治疗OVX雌性大鼠短暂前脑缺血(30分钟的右颈总动脉闭塞和出血性低血压)和再灌注。粘附的罗丹明-6G标记的白细胞,通过一个封闭的颅窗观察使用活体显微镜。缺血前和不同时间后reperfusion.Results-Before白细胞粘附测定缺血前,白细胞粘附(粘附白细胞所占的小静脉面积的百分比测量)是2至3倍以上的OVX与完整的或E2处理的OVX大鼠(7.0%,3.4%,和2.2%,分别)。再灌注120分钟后,这种差异消失,此时在所有组中观察到相当水平的白细胞粘附增强。在去卵巢大鼠中,白细胞粘附在再灌注4和6小时后仍然升高(分别为11.6%和12.9%),而其他两组则明显低于(未处理大鼠为5.0%和5.8%,E2处理的OVX大鼠为7.0%和7.2%)。目前的研究结果表明,雌激素调节白细胞粘附在脑循环短暂前脑缺血后。这种作用表明,减少白细胞粘附可能是雌激素介导的神经保护的一个重要机制。
Background and Purpose—Recent findings indicate that estrogen (ie, 17β-estradiol [E2]) provides neuroprotection in models of transient global and focal ischemia. Enhanced postischemic leukocyte adhesion and infiltration have been linked to neuropathology in the brain as well as other tissues. We recently showed that estrogen reduces leukocyte adhesion in the cerebral circulation of female rats during resting conditions.Methods—We compared leukocyte adhesion in pial venules in vivo in intact, ovariectomized (OVX), and E2-treated OVX female rats subjected to transient forebrain ischemia (30-minute right common carotid artery occlusion and hemorrhagic hypotension) and reperfusion. Adherent rhodamine-6G–labeled leukocytes were viewed through a closed cranial window with the use of intravital microscopy. Leukocyte adhesion was measured before ischemia and at different times after reperfusion.Results—Before ischemia, leukocyte adhesion (measured as a percentage of venular area occupied by adherent leukocytes) was 2 to 3 times greater in OVX versus intact or E2-treated OVX rats (7.0%, 3.4%, and 2.2%, respectively). This difference disappeared at 120 minutes of reperfusion, when comparable levels of enhanced leukocyte adhesion were observed in all groups. In OVX rats, leukocyte adhesion remained elevated after 4 and 6 hours of reperfusion (11.6% and 12.9%, respectively), while the other 2 groups showed significantly lower levels (5.0% and 5.8% for intact rats and 7.0% and 7.2% for E2-treated OVX rats).Conclusions—Present results demonstrate that estrogen modulates leukocyte adhesion in the cerebral circulation after transient forebrain ischemia. This effect suggests that decreased leukocyte adhesion may be an important mechanism in estrogen-mediated neuroprotection.