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| بین المللی علوم (منتشر نمی شود) | ||
| مقاله 2، دوره 6، شماره 0 - شماره پیاپی 1374، اردیبهشت 1384 اصل مقاله (1.57 M) | ||
| نویسندگان | ||
| S. Abbasi؛ A. Parvaneh Tafreshi؛ H. Sepehri؛ F. Sabooni؛ B. Zeynali* | ||
| عنوان مقاله [English] | ||
| - | ||
| چکیده [English] | ||
| Nerve growth factor (NGF) is the first characterized member of the neurotrophin family. It is known for its crucial role in survival, differentiation and maintenance of neurons both in peripheral and central nervous system. In addition to its neurotrophic role, NGF has been also proposed to influence the immune system. Recent studies indicate that in multiple sclerosis and in its animal model (EAE) there is an increased level of NGF in acute phase of the disease (relapses) and conversely decreased level during the remission phase. Increased level of NGF has been also reported in other autoimmune diseases such as lupus erythmatosus. Concomitantly, proinflammatory cytokines are upregulated in the acute phase of autoimmune diseases, known to be as potent inducers of heat shock protein expression. These observations suggest that over production of NGF in CNS may functionally be related to the state of activation of the immune system in autoimmune diseases. In this study, we have investigated whether increased level of NGF in CNS triggers the immune system. NGF was therefore injected intracerebroventricularly at doses 5 and 20??g/mice for four days. Our histological and immunohistochemical results show that there are no signs of immune cell infiltration and no changes in the level of heat shock protein expression in different areas of the brain. We therefore suggest that either NGF alone is unable to trigger the immune system or the NGF regimen used in this study was insufficient to do so. | ||
| کلیدواژه‌ها [English] | ||
| CNS, heat shock protein, ICV, NGF | ||
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