ANTI-ICAM-1 ANTIBODY TREATMENT AFTER MCA OCCLUSION
MCA 闭塞后抗 ICAM-1 抗体治疗
基本信息
- 批准号:2655495
- 负责人:
- 金额:$ 22.87万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:1995
- 资助国家:美国
- 起止时间:1995-02-01 至 1999-01-31
- 项目状态:已结题
- 来源:
- 关键词:artery occlusion autoradiography blocking antibody brain circulation cell adhesion molecules cerebral ischemia /hypoxia cerebrovascular occlusions gene expression histology immunocytochemistry immunotherapy laboratory rat magnetic resonance imaging monoclonal antibody neutrophil northern blottings nuclear magnetic resonance spectroscopy reperfusion
项目摘要
Ischemic brain injury evokes an endogenous brain parenchymal cell damage
as well as an exogenous inflammatory response, which includes infiltration
and accumulation of polymorphonuclear leukocytes and
monocytes/macrophages, and microvascular proliferation. The migration and
accumulation of neutrophils into the ischemic tissue after reperfusion is
not only associated with tissue repair processes, but also may result in
injury to potentially viable tissue. We propose to reduce ischemic cell
damage after middle cerebral artery (MCA) occlusion in the rat by
selectively blocking the intercellular adhesion molecule 1 (ICAM-1), a
glycoprotein expressed on endothelial cells that facilitates leukocyte
adhesion. Three specific aims and hypotheses will be tested.
Aim 1: The effect of administration of a monoclonal antibody to the rat
ICAM-1 on reducing ischemic cell damage will be investigated in rats
subjected to transient (2 hours) and permanent MCA occlusion. Ischemic
cell damage will be measured as a function of dose and time of antibody
administration.
Hypothesis: A monoclonal antibody reactive with the ICAM-1 glycoprotein
reduces ischemic cell damage after transient MCA occlusion.
Aim 2: We will measure the temporal profiles of expression of ICAM-1 and
ICAM-1 mRNA in brain after transient MCA occlusion.
Hypothesis: MCA occlusion results in an increase of both ICAM-1 message
and protein in ischemic brain.
Aim 3: Mechanisms by which the anti-ICAM-1 reactive antibody reduces
ischemic cell damage will be investigated. 3(a): We will measure and
correlate the temporal profile of the extent of neutrophil infiltration
into the ischemic tissue with ischemic cell damage.
Hypothesis: Anti-ICAM-1 antibody causes a reduction of neutrophils in the
ischemic tissue. Infiltration of neutrophils into the ischemic tissue
precedes or is concomitant with ischemic cell damage, and contributes to
ischemic cell damage after transient focal cerebral ischemia.
We will perform quantitative autoradiographic measurements of local
cerebral blood flow at time points after transient MCA occlusion.
Hypothesis: Neutrophils may contribute to ischemic cell damage in
reperfusion injury by reducing local cerebral blood flow (CBF) and
extending the duration of ischemia.
Our long term objective is to develop a therapeutic intervention (anti-
ICAM-1 antibody) to be employed after the onset of ischemic stroke.
缺血性脑损伤引起内源性脑实质细胞损伤
项目成果
期刊论文数量(0)
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会议论文数量(0)
专利数量(0)
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