کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
9436531 | 1615694 | 2005 | 13 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Protective effect of T-type calcium channel blocker flunarizine on cisplatin-induced death of auditory cells
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کلمات کلیدی
NACFlunarizineDulbecco’s modified essential mediumOHCGSHFBSDMEM3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide - 3- (4،5-dimethylthiazol-2-yl) -2،5-difenyl tetrazolium bromideMTT - MTTN-acetylcysteine - N-استیل سیستئینorgan of Corti - اندام کورتیIHC - ایمونوهیستوشیمیTUNEL - تونلfetal bovine serum - سرم جنین گاوOuter hair cells - سلول های موی بیرونیinner hair cells - سلول های موی درونیOtotoxicity - سمیت زایی برای گوش، اتوتوکسیسیتیcisplatin - سیس پلاتینGlutathione - گلوتاتیون
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
سیستم های حسی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Protective effect of T-type calcium channel blocker flunarizine on cisplatin-induced death of auditory cells Protective effect of T-type calcium channel blocker flunarizine on cisplatin-induced death of auditory cells](/preview/png/9436531.png)
چکیده انگلیسی
Changes in intracellular Ca2+ level are involved in a number of intracellular events, including triggering of apoptosis. The role of intracellular calcium mobilization in cisplatin-induced hair cell death, however, is still unknown. In this study, the effect of calcium channel blocker flunarizine (Sibeliumâ¢), which is used to prescribe for vertigo and tinnitus, on cisplatin-induced hair cell death was investigated in a cochlear organ of Corti-derived cell line, HEI-OC1, and the neonatal (P2) rat organ of Corti explant. Cisplatin induced apoptotic cell death showing nuclear fragmentation, DNA ladder, and TUNEL positive in both HEI-OC1 and primary organ of Corti explant. Flunarizine significantly inhibited the cisplatin-induced apoptosis. Unexpectedly, flunarizine increased the intracellular calcium ([Ca2+]i) levels of HEI-OC1. However, the protective effect of flunarizine against cisplatin was not mediated by modulation of intracellular calcium level. Treatment of cisplatin resulted in ROS generation and lipid peroxidation in HEI-OC1. Flunarizine did not attenuate ROS production but inhibited lipid peroxidation and mitochondrial permeability transition in cisplatin-treated cells. This result suggests that the protective mechanism of flunarizine on cisplatin-induced cytotoxicity is associated with direct inhibition of lipid peroxidation and mitochondrial permeability transition.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Hearing Research - Volume 204, Issues 1â2, June 2005, Pages 127-139
Journal: Hearing Research - Volume 204, Issues 1â2, June 2005, Pages 127-139
نویسندگان
Hong-Seob So, Channy Park, Hyung-Jin Kim, Jung-Han Lee, Sung-Yeol Park, Jai-Hyung Lee, Zee-Won Lee, Hyung-Min Kim, Federico Kalinec, David J. Lim, Raekil Park,