NDLI: Reperfusion Therapy for Acute Stroke Improves Outcome by Decreasing Neuroinflammation

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Proteomic Protease Substrate Profiling of tPA Treatment in Acute Ischemic Stroke Patients: A Step Toward Individualizing Thrombolytic Therapy at the Bedside

Proteomic Identification of Novel Plasma Kallikrein Substrates in the Astrocyte Secretome

MicroRNAs in Cerebral Ischemia

Assessing the Quality and Reproducibility of a Proteomic Platform for Clinical Stroke Biomarker Discovery

Translational Stroke Research : Volume 1, Issue 3, September 2010

Translational Stroke Research : Volume 1, Issue 2, June 2010

Translational Stroke Research : Volume 1, Issue 1, March 2010

Reperfusion Therapy for Acute Stroke Improves Outcome by Decreasing Neuroinflammation

Content Provider	Springer Nature Link
Author	Montaner, Joan Salat, David García Berrocoso, Teresa Molina, Carlos A. Chacón, Pilar Ribó, Marc Alvarez Sabín, José Rosell, Anna
Copyright Year	2010
Abstract	Inflammation is a major step in the ischemic cascade, and proinflammatory cytokines, adhesion molecules and chemokines have been related to brain injury after stroke. To investigate if tissue plasminogen activator (tPA) treatment decreases the deleterious neuroinflammatory response that follows ischemic stroke. Our target population was 80 patients with ischemic stroke involving the middle cerebral artery (MCA) territory. Among them, 41 received tPA within 3 h of symptom onset according to National Institute of Neurological Disorders and Stroke recommendations and the remaining 39 were assessed prior to local approval of tPA. In all patients, blood samples were obtained at 12 and 24 h after symptom onset. Serum determinations of interleukin (IL)-6, inter-cellular adhesion molecule 1 (ICAM-1), IL-8 and tumor necrosis factor-alpha (TNF-α) were obtained by ELISA. National Institutes of Health Stroke Scale (NIHSS) and transcranial Doppler recordings (proximal/distal occlusion, p.o/d.o) were obtained at baseline and follow-up. No differences were found between the two groups in baseline NIHSS scores (tPA = 17 and control = 17; p = 0.38) or MCA status (tPA: p.o = 65.8%, control: p.o = 55.3%; p = 0.41). We found a lower level of mean IL-6 and IL-8 in the tPA treatment group: IL-6 (14.06 vs. 37.88 pg/ml, p = 0.001) and IL-8 (70.98 vs. 465 pg/ml, p < 0.001). No significant changes appeared for ICAM-1 and TNF-α. This biological response was accompanied by a neurological improvement (24 h NIHSS: tPA = 11 and control = 15; p = 0.024) and a mortality reduction (tPA = 9.75% vs. controls = 28.2%; p = 0.038). Patients who improved and those who recanalised had the lowest IL-6 levels (p < 0.005). tPA treatment reduces the severity of the inflammatory phenomena that follows stroke. These results may partially explain the efficacy of reperfusion therapy on stroke outcome.
Starting Page	261
Ending Page	267
Page Count	7
File Format	PDF
ISSN	18684483
Journal	Translational Stroke Research
Volume Number	1
Issue Number	4
e-ISSN	1868601X
Language	English
Publisher	Springer-Verlag
Publisher Date	2010-08-28
Publisher Place	New York
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Cerebral ischemia Cytokines Embolic Inflammation Plasmin Stroke tPA Thrombolysis Vascular Surgery Neurosurgery Cardiology Neurology Neurosciences
Content Type	Text
Resource Type	Article
Subject	Cardiology and Cardiovascular Medicine Neuroscience Neurology (clinical)

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