کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6016339 | 1579943 | 2008 | 6 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Changes in sphingomyelinases, ceramide, Bax, Bcl2, and caspase-3 during and after experimental status epilepticus
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
عصب شناسی
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چکیده انگلیسی
Status epilepticus (SE) induces a number of events leading to programmed cell death (PCD). The aim of our work is to study the time sequence of activation of different factors in experimental SE (intraperitoneal kainic acid (KA) model). We studied ceramide, a known mediator of apoptosis in multiple models, sphingomyelinases (SMases), enzymes that break down sphingomyelin and increase ceramide thus leading to apoptosis in many models, Bcl2, Bax, and caspase-3. SE induced a sustained ceramide increase starting 2Â h after kainic acid injection followed by an increase in Bax protein at 6 and 12Â h, and the appearance of caspase-3-activated fragment (caspase-3a) immunostaining and TUNEL positivity at 12Â h. Status epilepticus also induced an increase in acidic and neutral sphingomyelinases that preceded (acidic sphingomyelinase) and parallelled (acidic and neutral sphingomyelinase) the increases in ceramide. These data suggest that, in this model, Bax is activated early in the process and that its increase is sustained till 12Â h after kainic acid injection which is the time of first appearance of caspase-3 activation and TUNEL positivity, and that SMases contribute to increases in ceramide levels during and after status epilepticus.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Epilepsy Research - Volume 81, Issues 2â3, October 2008, Pages 161-166
Journal: Epilepsy Research - Volume 81, Issues 2â3, October 2008, Pages 161-166
نویسندگان
Mohamad A. Mikati, Michele Zeinieh, Ralph Abi Habib, Jimmy El Hokayem, Amal Rahmeh, Marwan El Sabban, Julnar Usta, Ghassan Dbaibo,