کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8348170 | 1541716 | 2015 | 8 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Neuroprotective effects of apelin-13 on experimental ischemic stroke through suppression of inflammation
ترجمه فارسی عنوان
اثرات ضد عفونی آپلین 13 بر سکته مغزی ایسکمیک تجربی از طریق سرکوب التهاب
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کلمات کلیدی
IBA1MCAOIL-1βHMGB1GFAPICAM-1MPO - DFOI/R - I / Rinflammation - التهاب( توروم) middle cerebral artery occlusion - انسداد شریان (سرخرگ) مغزی میانیischemia/reperfusion - ایسکمی / رپرفیوژنCerebral ischemia - ایسکمی مغزیInterleukin-1β - اینترلوکین-1βtumor necrosis factor-α - تومور نکروز عامل αApelin-13 - درخواست تجدید نظر، 13TNF-α - فاکتور نکروز توموری آلفاNeuroprotection - محافظت نورونی یا محافظت از عصبintercellular adhesion molecule-1 - مولکول چسبندگی بین سلولی -1ionized calcium-binding adapter molecule-1 - مولکول-آداپتور اتصال دهنده کلسیم یونیزه-1myeloperoxidase - میلوپراکسیداز Glial fibrillary acidic protein - پروتئین اسیدی فیبریلاسیون گلایالHigh mobility group box 1 - کادر تحرک بالا 1
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
چکیده انگلیسی
Acute inflammation plays an important role in the pathogenic progression of post-ischemic neuronal damage. Apelin-13 has been investigated as a neuropeptide for various neurological disorders. The present study was performed to evaluate the effects of apelin-13 on the inflammation of cerebral ischemia/reperfusion (I/R) injury. Transient focal I/R model in male Wistar rats were induced by 2 h middle cerebral artery occlusion (MCAO) followed by 24 h reperfusion. Rats then received treatment with apelin-13 or vehicle after ischemia at the onset of reperfusion. The neurological deficit was evaluated and the infarct volume was measured by TTC staining. The activity of myeloperoxidase (MPO) was measured. The expression of pro-inflammatory cytokines including tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and intercellular adhesion molecule-1 (ICAM-1) were measured using real-time PCR. And the expression of apelin receptor (APJ), ionized calcium-binding adapter molecule-1 (Iba1), glial fibrillary acidic protein (GFAP) and high mobility group box 1 (HMGB1) were measured by immunohistochemistry and western blot. Our results demonstrated that treatment with apelin-13 in I/R rats markedly reduced neurological deficits and the infarct volume. The increase of MPO activity induced by I/R was inhibited by apelin-13 treatment. The real-time PCR showed that apelin-13 decreased the expression of inflammatory cytokines such as IL-1β, TNF-α and ICAM-1 in I/R rats. The expression of APJ in I/R rats was increased. And the expression of Iba1, GFAP and HMGB1 in I/R rats was decreased by apelin-13 treatment indicating the inhibition of microglia, astrocytes and other inflammatory cells. In conclusion, apelin-13 is neuroprotective for neurons against I/R through inhibiting the neuroinflammation.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Peptides - Volume 63, January 2015, Pages 55-62
Journal: Peptides - Volume 63, January 2015, Pages 55-62
نویسندگان
Qing Xin, Baohua Cheng, Yanyou Pan, Haiqing Liu, Chunqing yang, Jing Chen, Bo Bai,