دورية أكاديمية

Antagonism of leukocyte adherence by synthetic fibronectin peptide V in a rat model of transient focal cerebral ischemia.

التفاصيل البيبلوغرافية
العنوان: Antagonism of leukocyte adherence by synthetic fibronectin peptide V in a rat model of transient focal cerebral ischemia.
المؤلفون: Yanaka K; Department of Neurosurgery, University of Minnesota Medical School, Minneapolis, USA., Camarata PJ, Spellman SR, McCarthy JB, Furcht LT, Low WC
المصدر: Neurosurgery [Neurosurgery] 1997 Mar; Vol. 40 (3), pp. 557-63; discussion 563-4.
نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
اللغة: English
بيانات الدورية: Publisher: Lippincott Williams & Wilkins, Inc Country of Publication: United States NLM ID: 7802914 Publication Model: Print Cited Medium: Print ISSN: 0148-396X (Print) Linking ISSN: 0148396X NLM ISO Abbreviation: Neurosurgery Subsets: MEDLINE
أسماء مطبوعة: Publication: 2022- : [Philadelphia] : Lippincott Williams & Wilkins, Inc.
Original Publication: Baltimore, Williams & Wilkins.
مواضيع طبية MeSH: Leukocyte Adherence Inhibition Test*, Fibronectins/*pharmacology , Ischemic Attack, Transient/*immunology , Peptide Fragments/*pharmacology, Animals ; Brain Damage, Chronic/immunology ; Cerebral Infarction/immunology ; Dose-Response Relationship, Drug ; Leukocyte Count/drug effects ; Leukocytes/drug effects ; Leukocytes/immunology ; Male ; Neurologic Examination/drug effects ; Peroxidase/metabolism ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury/immunology
مستخلص: Objective: Activated polymorphonuclear leukocytes (PMNs) seem to be directly involved in potentiating ischemic brain injury. Recent work in our laboratory demonstrated that synthetic fibronectin peptides significantly inhibit PMN accumulation in ischemic tissue, reduce the size of infarction, and reduce neurological dysfunction after transient focal cerebral ischemia in rats. The purpose of this study was to examine any dose-related effects (Experiment 1) and the optimal timing of the administration (Experiment 2) of synthetic fibronectin peptide V (FN-C/H-V) to further substantiate the role of the peptide in ameliorating cerebral ischemic damage.
Methods: Fifty-six animals were included in the study. We evaluated the efficacy of FN-C/H-V on PMN accumulation in ischemic tissue, infarct size, and neurological outcomes in rats subjected to 1 hour of cerebral ischemia and 48 hours of reperfusion.
Results: In Experiment 1, the animals receiving FN-C/H-V at a dose of 10 to 15 mg/kg of body weight per injection showed significant reduction of PMN accumulation, reduction of infarct size, and improvement of neurological outcomes at 48 hours after reperfusion compared to untreated animals (P < 0.05). In Experiment 2, the animals receiving FN-C/H-V within 3 hours after reperfusion also showed significantly better results than untreated animals (P < 0.05). Despite the treatment delay, the administration of FN-C/H-V inhibited PMN accumulation after reperfusion but did not reduce the size of infarction when administered 6 hours after reperfusion.
Conclusion: These data suggest that relatively late postischemic administration of FN-C/H-V is effective in brain protection after ischemia/reperfusion.
معلومات مُعتمدة: 1 K08-NS 01745-01 United States NS NINDS NIH HHS
المشرفين على المادة: 0 (Fibronectins)
0 (Peptide Fragments)
EC 1.11.1.7 (Peroxidase)
تواريخ الأحداث: Date Created: 19970301 Date Completed: 19970604 Latest Revision: 20190512
رمز التحديث: 20231215
DOI: 10.1097/00006123-199703000-00026
PMID: 9055296
قاعدة البيانات: MEDLINE
الوصف
تدمد:0148-396X
DOI:10.1097/00006123-199703000-00026