کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
4340109 1295783 2009 8 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Thalidomide inhibition of vascular remodeling and inflammatory reactivity in the quinolinic acid–injected rat striatum
موضوعات مرتبط
علوم زیستی و بیوفناوری علم عصب شناسی علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله
Thalidomide inhibition of vascular remodeling and inflammatory reactivity in the quinolinic acid–injected rat striatum
چکیده انگلیسی

Effects of thalidomide administration on vascular remodeling, gliosis and neuronal viability have been studied in excitotoxin-injected rat striatum. Intrastriatal injection of quinolinic acid (QUIN) caused time-dependent changes (durations of 6 h, 1 and 7 d post-injection) in vascular remodeling. QUIN excitotoxic insult was associated with increased numbers of vessels (laminin or collagen IV markers) demonstrating considerable abnormalities in morphology, including short fragments and vascular loops. Non-lesioned striatum, with injection of phosphate buffer solution (PBS) as a vehicle, showed no evidence for vascular remodeling. A maximal extent of vascular remodeling was measured at 1 d post-QUIN and was correlated with marked increases in microgliosis (ED1 marker) and astrogliosis (glial fibrillary acidic protein [GFAP] marker) relative to control PBS injection. Double staining of laminin with ED1 and GFAP demonstrated areas of close association of glial cells with blood vessels. Treatment of QUIN-injected animals with the anti-inflammatory compound, thalidomide significantly inhibited vascular remodeling (by 43%) and reduced microgliosis (by 33%) but was ineffective in modifying extents of astrogliosis. Intrastriatal QUIN injection was associated with a marked loss of striatal neurons relative to non-lesioned control with thalidomide treatment exhibiting a significant degree of neuroprotection (24% recovery) against QUIN-induced neurotoxicity. These results suggest close links between microglial-mediated inflammatory responses and vascular remodeling, with inflammatory reactivity associated with, and contributing to, neuronal damage in excitotoxically-lesioned striatum.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience - Volume 163, Issue 2, 6 October 2009, Pages 601–608
نویسندگان
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