کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
6278912 1296532 2016 10 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Research articlePost-ischemia mdivi-1 treatment protects against ischemia/reperfusion-induced brain injury in a rat model
موضوعات مرتبط
علوم زیستی و بیوفناوری علم عصب شناسی علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله
Research articlePost-ischemia mdivi-1 treatment protects against ischemia/reperfusion-induced brain injury in a rat model
چکیده انگلیسی


- Post-ischemia mdivi-1 treatment decreased infarct volume and improved neurological function.
- Post-ischemia mdivi-1 treatment reduced apoptosis in cerebral cortex tissue.
- Post-ischemia mdivi-1 treatment inhibited mitochondrial fragmentation.
- Post-ischemia mdivi-1 treatment attenuated translocation of Drp1 protein to the mitochondria.
- Post-ischemia mdivi-1 treatment enhanced I/R-induced mitochondrial biogenesis.

When given prior to brain ischemia, mitochondrial division inhibitor-1 (mdivi-1) attenuates the brain damage caused by ischemia. Here, we investigated the potential effects of post-ischemia mdivi-1 treatment (1 mg/kg, i.p., administered immediately after 2 h of ischemia and prior to reperfusion) using a MCAO rat model. Mdivi-1 treatment decreased infarct volume and improved neurological function. In addition, cytochrome C release was attenuated, and neuronal apoptosis was decreased. The mitochondrial fission protein dynamin-related protein 1 (Drp1) was decreased in the mitochondrial fraction but increased in the cytosolic fraction. Mdivi-1 treatment augmented the increases in the mRNA expression of peroxisome proliferator-activated receptor coactivator-1α, nuclear respiratory factor-1, and mitochondrial transcriptional factor A. In conclusion, when given after ischemia and prior to reperfusion, mdivi-1 can protect against brain damage by inhibiting the mitochondria-mediated apoptosis induced by mitochondrial fission. Post-ischemia mdivi-1 treatment might promote I/R-induced mitochondrial biogenesis.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience Letters - Volume 632, 6 October 2016, Pages 23-32
نویسندگان
, , , , , ,