کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8838985 | 1613220 | 2018 | 28 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
The phosphodiesterase-4 inhibitor, FCPR16, attenuates ischemia-reperfusion injury in rats subjected to middle cerebral artery occlusion and reperfusion
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کلمات کلیدی
MCAO/RPDE4IL-6IL-1βpKaGFAPCREBTTCBcl-2cAMP - cAMPH&E - H & EIba-1 - IBA-1Cyclic adenosine monophosphate - آدنوزین مونوفسفات CyclicIschemia-reperfusion injury - آسیب ایسکمی ـ باز خون رسانی یا آسیب ناشی از ایسکمی و برقراری مجدد جریان خونinflammation - التهاب( توروم) Middle cerebral artery occlusion and reperfusion - انسداد سرخرگ مغزی و رپرفیوژنinterleukin-6 - اینترلوکین ۶Interleukin-1β - اینترلوکین-1βBax - باکسtumor necrosis factor α - تومور نکروز عامل αApoptosis - خزان یاختهایCNS - دستگاه عصبی مرکزیStroke - سکته مغزیcentral nervous system - سیستم عصبی مرکزیTNF-α - فاکتور نکروز توموری آلفاphosphodiesterase-4 - فسفودی استراز 4B-cell lymphoma-2 - لنفوم سلول B-2ionized calcium-binding adapter molecule 1 - ملکول آداپتور اتصال دهنده کلسیم یونیزه 1PDE4 inhibitor - مهار کننده PDE4haematoxylin and eosin - هماتوکسیلین و ائوزینBcl-2 Associated X protein - پروتئین Bcl-2 Associated XcAMP-response element binding protein - پروتئین اتصال دهنده عنصر cAMPGlial fibrillary acidic protein - پروتئین اسیدی فیبریلاسیون گلایالcAMP-dependent protein kinase A - پروتئین کیناز A وابسته به cAMP
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب سلولی و مولکولی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Current phosphodiesterase-4 (PDE4) inhibitors exert beneficial effects in central nervous system diseases via anti-inflammatory and anti-apoptotic properties, but many of them are plagued by side effects like nausea and emesis. FCPR16, a novel PDE4 inhibitor synthesized in our lab, has potential anti-inflammatory property. In the present study, we aimed to investigate the effects of FCPR16 in a rat model of ischemic stroke and evaluate its emetogenic potential. Our results showed that FCPR16 treatment improved neurological function, reduced cerebral infarct volume, and attenuated brain histological changes in rats subjected to middle cerebral artery occlusion and reperfusion (MCAO/R). Furthermore, levels of proinflammatory cytokines tumor necrosis factor α, interleukin-6 and interleukin-1β were decreased after FCPR16 treatment, as well as the ionized calcium-binding adapter molecule 1 and glial fibrillary acidic protein in MCAO/R rats. TUNEL staining and Western blot results showed that FCPR16 reduced apoptosis and regulated apoptotic-related proteins, with increased level of phosphorylated protein kinase B. Moreover, FCPR16 treatment increased cyclic adenosine monophosphate (cAMP) levels and cAMP-response element binding protein (CREB) phosphorylation in ischemic tissue. In addition, oral administration of 3 mg/kg FCPR16 did not cause vomiting in beagle dogs. This study indicates that FCPR16 has protective effects against cerebral ischemia-reperfusion injury through inhibiting inflammation and apoptosis via the cAMP/CREB pathway, while it has low emetogenic potential.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Brain Research Bulletin - Volume 137, March 2018, Pages 98-106
Journal: Brain Research Bulletin - Volume 137, March 2018, Pages 98-106
نویسندگان
Jiajia Chen, Hui Yu, Jiahong Zhong, Hongfang Feng, Haitao Wang, Yufang Cheng, Zhengqiang Zou, Chang Huang, Zhongzhen Zhou, Wenhua Zheng, Jiangping Xu,