کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
4327408 | 1614129 | 2010 | 8 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Opioid growth factor suppresses expression of experimental autoimmune encephalomyelitis
دانلود مقاله + سفارش ترجمه
دانلود مقاله ISI انگلیسی
رایگان برای ایرانیان
کلمات کلیدی
CFAMOGPHAGFAPEAEOGFrphytohemagglutincomplete Freund's adjuvant - adjuvant دوست کاملOpioid - opioidexperimental autoimmune encephalomyelitis - آنسفالومیلیت خودایمنی تجربیAutoimmune diseases - بیماری خودایمنیOpioid growth factor - عامل رشد اپیوئیدMultiple sclerosis - مولتیپل اسکلروزیس(ام اس)Glial fibrillary acidic protein - پروتئین اسیدی فیبریلاسیون گلایالmyelin oligodendrocyte glycoprotein - گلیکوپروتئین الیگودندروسیت میلینOpioid growth factor receptor - گیرنده عامل فاکتور رشد اپوئیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Opioid growth factor suppresses expression of experimental autoimmune encephalomyelitis Opioid growth factor suppresses expression of experimental autoimmune encephalomyelitis](/preview/png/4327408.png)
چکیده انگلیسی
Naltrexone, an opioid antagonist, has been shown to modulate expression of experimental autoimmune encephalomyelitis (EAE), an animal model of MS, suggesting that endogenous opioids are inhibitory trophic factors in EAE. In the present study, we investigated the effects of one native opioid peptide, opioid growth factor ([Met5]-enkephalin), on the onset and progression of EAE. C57Bl/6 mice injected with myelin oligodendrocyte glycoprotein (MOG) received daily injections of 10Â mg/kg OGF (MOGÂ +Â OGF) or saline (MOGÂ +Â Vehicle). Over 60% of the MOGÂ +Â OGF animals did not exhibit behavioral signs of disease (EAE) in contrast to 100% of the mice in the MOGÂ +Â Vehicle group. The severity and disease indices of EAE in the OGF-treated mice were markedly reduced from MOGÂ +Â Vehicle cohorts. By day 30, 60% of MOGÂ +Â OGF mice had a remission, relative to 4% in the MOGÂ +Â Vehicle group. MOG-injected mice receiving OGF had significant reductions in activated astrocytes and damaged neurons compared to MOGÂ +Â Vehicle animals. Unlike MOGÂ +Â Vehicle and MOGÂ +Â OGF mice with behavioral signs of disease, MOGÂ +Â OGF animals without manifestation of disease had no lumbar spinal cord demyelination. Both OGF and OGF receptor were detected in splenic-derived T lymphocytes by immunohistochemistry. OGF treatment decreased both DNA synthesis and cell proliferation in comparison to vehicle-treated T cell lymphocyte cultures. These results indicate that an endogenous opioid, OGF, inhibits the onset and progression of EAE, and suggest that clinical studies on the use of OGF treatment for MS are merited.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Brain Research - Volume 1310, 15 January 2010, Pages 154-161
Journal: Brain Research - Volume 1310, 15 January 2010, Pages 154-161
نویسندگان
Ian S. Zagon, Kristen A. Rahn, Robert H. Bonneau, Anthony P. Turel, Patricia J. McLaughlin,