کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8278535 | 1535126 | 2014 | 9 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Ischemic preconditioning-induced neuroprotection against transient cerebral ischemic damage via attenuating ubiquitin aggregation
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
سالمندی
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چکیده انگلیسی
Ubiquitin binds to short-lived proteins, and denatured proteins are produced by various forms of injuries. In the present study, we investigated the effect of ischemic preconditioning (IPC) on free ubiquitin and its mutant form (ubiquitin+Â 1) in the gerbil hippocampus induced by transient cerebral ischemia. The animals were randomly assigned to 4 groups (sham-operated-group, ischemia-operated-group, IPC plus (+)-sham-operated-group, and IPCÂ +Â ischemia-operated-group). IPC was induced by subjecting gerbils to a 2Â min of ischemia followed by 1Â day of recovery. A significant loss of neurons was observed in the stratum pyramidale (SP) of the hippocampal CA1 region (CA1) in the ischemia-operated-groups 5Â days after ischemia-reperfusion (I-R). In all the IPCÂ +Â ischemia-operated-groups, neurons in the SP were well protected. We found that strong ubiquitin immunoreactivity was detected in the SP in the sham-operated-group and the immunoreactivity was decreased with time after I-R. In all the IPCÂ +Â ischemia-operated-groups, ubiquitin immunoreactivity in the SP was similar to that in the sham-operated group. Moderate ubiquitin+Â 1 immunoreactivity was detected in the SP of the sham-operated-group, and the immunoreactivity was markedly increased 2Â days after I-R. Five days after I-R, ubiquitin+Â 1 immunoreactivity was very weak in the SP. In all the IPCÂ +Â ischemia-operated-groups, ubiquitin+Â 1 immunoreactivity in the SP was slightly decreased with time after I-R. Western blot analysis showed that, in all the IPCÂ +Â ischemia-ischemia-groups, the levels of ubiquitin and ubiquitin+Â 1 proteins were well maintained after I-R. In brief, our findings suggest that the inhibition of the depletion of free ubiquitin and the formation of ubiquitin+Â 1 may have an essential role in inducing cerebral ischemic tolerance by IPC.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Journal of the Neurological Sciences - Volume 336, Issues 1â2, 15 January 2014, Pages 74-82
Journal: Journal of the Neurological Sciences - Volume 336, Issues 1â2, 15 January 2014, Pages 74-82
نویسندگان
Jae-Chul Lee, In Hye Kim, Geum-Sil Cho, Joon Ha Park, Ji Hyeon Ahn, Bing Chun Yan, Hyuk Min Kwon, Young-Myeong Kim, Seung Hwan Cheon, Jun Hwi Cho, Hui Young Lee, Moo-Ho Won, Jeong Yeol Seo,