The Effects of Arundic Acid on the Released S100B from Astrocytes and the Evaluation of This Effect on the Protection of Astrocytes against Beta-Amyloid in the Cell Culture
- سال انتشار: 1397
- محل انتشار: اولین کنگره بین المللی علوم اعصاب (نوروتکنولوژی و نقشه برداری مغزی)
- کد COI اختصاصی: NSMED01_039
- زبان مقاله: انگلیسی
- تعداد مشاهده: 522
نویسندگان
Department of Biochemistry, college of Agriculture, New Sciences and Technology Islamic Azad University, Shiraz Branch, Shiraz, Iran
Shiraz Neuroscience Research Center, Shiraz University of Medical sciences, Shiraz, Iran
Department of Biochemistry, college of Agriculture, New Sciences and Technology Islamic Azad University, Shiraz Branch, Shiraz, Iran
چکیده
Recent studies have shown that the activation of glia cells, especially astrocytes by beta-amyloid is important in the progression of Alzheimer’s disease. The S100B is an astrocyte specific factor that may damage the cells of the central nervous system. Arundic acid is a compound that prevents the production and secretion of S100B. The aim of this study was to investigate the role of S100B in the cyto-protective effects of arundic acid against beta-amyloid in 1321N1 astrocyte cell culture. In this study, human astrocyte cells (1321N1) were treated with beta-amyloid (200 mM) and/or arundic acid (50 mM) for 24 hours. Cell death was measured using MTT (3, 4, 5-dimethylthiazole-2, 5-diphenyl tetrazolium bromide) method. The S100B protein was measured using the ELISA method.Beta-amyloid treatment reduced cell survival compared to the control-treated groups. In contrast, addition of arundic acid to beta-amyloid suppressed beta-amyloid induced cell death. Beta-amyloid also increased the S100B protein level. However, arundic acid prevented the rise of S100B protein level induced by beta-amyloid. Arundic acid protected astrocytes cells possible by suppression of S100B protein rising induced by beta-amyloid.کلیدواژه ها
Alzheimer disease; Amyloid beta-peptides; S100 Calcium binding protein beta subunit; ONO2506; Astrocytesمقالات مرتبط جدید
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