کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6022044 | 1580662 | 2014 | 7 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Isoflurane on brain inflammation
ترجمه فارسی عنوان
ایسفلوران بر التهاب مغز
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کلمات کلیدی
Phosphorylated c-Jun N-terminal kinaseBWCS1PSAHEBIIL-1βDMSvWFICAM-1COX-2SphKMPO - DFOIba-1 - IBA-1p-Jnk - p-jnkEarly brain injury - آسیب مغزی زودرسSphingosine kinase - اسپینوزین کینازsphingosine 1-phosphate - اسپینگزین 1-فسفاتinflammation - التهاب( توروم) Isoflurane - ایزوفلوران interleukin-1beta - اینترلوکین-1 بتاtumor necrosis factor-alpha - تومور نکروز عامل آلفاSubarachnoid hemorrhage - خونریزی زیر عنکبوتیهCyclooxygenase-2 - سیکلوکوکسیژناز2Von Willebrand factor - عامل فون ویلبراندTNF-α - فاکتور نکروز توموری آلفاbrain water content - محتوای مغز آبintercellular adhesion molecule-1 - مولکول چسبندگی بین سلولی -1ionized calcium binding adaptor molecule-1 - مولکول-1 متصل کننده کلسیم یونیزه شدهmyeloperoxidase - میلوپراکسیداز
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
عصب شناسی
چکیده انگلیسی
Brain inflammation may play an important role in the pathophysiology of early brain injury after subarachnoid hemorrhage (SAH). Our aim was to demonstrate brain inflammation development and to determine whether isoflurane, a clinically available volatile anesthetic agent, prevents brain inflammation after SAH. This study used 162 8-week-old male CD-1 mice. We induced SAH with endovascular perforation in mice and randomly assigned animals to sham-operated (n = 21), SAH + vehicle-air (n = 35) and SAH + 2% isoflurane (n = 31). In addition to the evaluation of brain injury (neurological scores, brain edema and Evans blue dye extravasation), brain inflammation was evaluated by means of expression changes in markers of inflammatory cells (ionized calcium binding adaptor molecule-1, myeloperoxidase), cytokines (tumor necrosis factor [TNF]-α, interleukin-1β), adhesion molecules (intercellular adhesion molecule [ICAM]-1, P-selectin), inducers of inflammation (cyclooxygenase-2, phosphorylated c-Jun N-terminal kinase [p-JNK]) and endothelial cell activation (von Willebrand factor) at 24 h post-SAH. Sphingosine kinase inhibitor (N, N-dimethylsphingosine [DMS]) and sphingosine-1-phosphate receptor-1/3 antagonist (VPC23019) were used to block isoflurane's effects (n = 22, each). SAH caused early brain injury, which was associated with inflammation so that all evaluated markers of inflammation were increased. Isoflurane significantly inhibited both brain injury (P < 0.001, respectively) and inflammation (myeloperoxidase, P = 0.022; interleukin-1β, P = 0.002; TNF-α, P = 0.015; P-selectin, P = 0.010; ICAM-1, P = 0.016; p-JNK, P < 0.001; cyclooxygenase-2, P = 0.003, respectively). This beneficial effect of isoflurane was abolished with DMS and VPC23019. Isoflurane may suppress post-SAH brain inflammation possibly via the sphingosine-related pathway.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neurobiology of Disease - Volume 62, February 2014, Pages 365-371
Journal: Neurobiology of Disease - Volume 62, February 2014, Pages 365-371
نویسندگان
Orhan Altay, Hidenori Suzuki, Yu Hasegawa, Robert P. Ostrowski, Jiping Tang, John H. Zhang,