کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
3070895 | 1580747 | 2007 | 8 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Re-evaluation of mitochondrial permeability transition as a primary neuroprotective target of minocycline
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کلمات کلیدی
Spinal cord injury - آسیب نخاعیamyotrophic lateral sclerosis - اسکلروز جانبی آمیوتروفیکIschemia - ایسکمیmotor neuron disease - بیماری نورون حرکتیHuntington’s disease - بیماری هانتینگتونParkinson’s disease - بیماری پارکینسونNeurodegeneration - تولید نوروژنیکApoptosis - خزان یاختهایCyclosporin - سیکلوسپورینNeuroprotection - محافظت نورونی یا محافظت از عصبBrain mitochondria - میتوکندری مغزیMinocycline - مینوسایکلین
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
عصب شناسی
پیش نمایش صفحه اول مقاله

چکیده انگلیسی
Minocycline has been shown to be neuroprotective in ischemic and neurodegenerative disease models and could potentially be relevant for clinical use. We revisited the hypothesis that minocycline acts through direct inhibition of calcium-induced mitochondrial permeability transition (mPT) resulting in reduced release of cytochrome c (cyt c). Minocycline, at high dosage, was found to prevent calcium-induced mitochondrial swelling under energized conditions similarly to the mPT inhibitor cyclosporin A (CsA) in rodent mitochondria derived from the CNS. In contrast to CsA, minocycline dose-dependently reduced mitochondrial calcium retention capacity (CRC) and respiratory control ratios and was ineffective in the de-energized mPT assay. Further, minocycline did not inhibit calcium- or tBid-induced cyt c release. We conclude that the neuroprotective mechanism of minocycline is likely not related to direct inhibition of mPT and propose that the mitochondrial effects of minocycline may contribute to toxicity rather than tissue protection at high dosing in animals and humans.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neurobiology of Disease - Volume 25, Issue 1, January 2007, Pages 198-205
Journal: Neurobiology of Disease - Volume 25, Issue 1, January 2007, Pages 198-205
نویسندگان
Roland MÃ¥nsson, Magnus J. Hansson, Saori Morota, Hiroyuki Uchino, Christine T. Ekdahl, Eskil Elmér,