کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
6264183 1613965 2012 9 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Research ReportLeonurine protects brain injury by increased activities of UCP4, SOD, CAT and Bcl-2, decreased levels of MDA and Bax, and ameliorated ultrastructure of mitochondria in experimental stroke
موضوعات مرتبط
علوم زیستی و بیوفناوری علم عصب شناسی علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله
Research ReportLeonurine protects brain injury by increased activities of UCP4, SOD, CAT and Bcl-2, decreased levels of MDA and Bax, and ameliorated ultrastructure of mitochondria in experimental stroke
چکیده انگلیسی

BackgroundIt has been proved that pre-treatment with leonurine could protect brain tissue against ischemic injury by exerting antioxidant effects and regulating mitochondrial function. Whether this protective effect applies to acute phase after cerebral ischemia, we therefore investigate the potential neuroprotective role of leonurine and the underlying mechanisms in cerebral ischemia. Methods: Focal cerebral ischemia was induced in adult male Sprague-Dawley rats by permanent middle cerebral artery occlusion (MCAO). Leonurine was administered intraperitoneally at 7.5 or 15 mg/kg/d at 2 h after surgery, then once daily thereafter. Neurological deficit, brain water content, and infarct volume were measured at 24 h, 72 h, and 7 d after stroke. Superoxide dismutase (SOD), catalase (CAT) activities, and malondialdehyde (MDA) content were also measured by spectrophotometer to evaluate oxidative reactions, and the expression of uncoupling protein 4 (UCP4), Bcl-2, and Bax were detected by reverse transcription-polymerase chain reaction (RT-PCR), immunohistochemical staining (IHC), and western blot, while the ultrastructure of the mitochondria were observed under transmission electron microscope. Results: Leonurine significantly alleviated neurological deficit, decreased brain water content and infarct volume after ischemic stroke, which was accompanied by decreased levels of MDA and Bax, increased activities of SOD, CAT, UCP4, and Bcl-2, and restored ultrastructure of mitochondria. Conclusions: The results showed that leonurine protected brain injury by increased activities of UCP4, SOD, CAT and Bcl-2, decreased levels of MDA and Bax, and ameliorated ultrastructure of mitochondria in experimental stroke.

► We evaluate the neuroprotection and mechanisms of leonurine after ischemia. ► Focal cerebral ischemia is induced in rats by permanent MCAO. ► Leonurine alleviates neurological deficit, brain edema and infarct size. ► Leonurine increases anti-oxidant and anti-apoptotic ability. ► Leonurine ameliorates ultrastructure of mitochondria.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Brain Research - Volume 1474, 20 September 2012, Pages 73-81
نویسندگان
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