این سایت در حال حاضر پشتیبانی نمی شود و امکان دارد داده های نشریات بروز نباشند
صفحه اصلی
درباره پایگاه
فهرست سامانه ها
الزامات سامانه ها
فهرست سازمانی
تماس با ما
JCR 2016
جستجوی مقالات
چهارشنبه 26 آذر 1404
Basic and Clinical Neuroscience
، جلد ۳، شماره ۲، صفحات ۴۷-۵۵
عنوان فارسی
چکیده فارسی مقاله
کلیدواژههای فارسی مقاله
عنوان انگلیسی
15-Deoxy-Δ12,14-Prostaglandin J2 Protects PC12 cells from LPS-Induced Cell Death Through Nrf2 pathway in PPAR-γ Dependent Manner
چکیده انگلیسی مقاله
Introduction: The inflammatory response requires a coordinated integration of various signaling pathway including cyclooxygenase (COX). COX catalyzes the formation of prostaglandins from arachidonic acid. Among prostaglandins, 15-Deoxy-D12, 14-prostaglandin J2 (15d-PGJ2), an endogenous ligand of Peroxisome proliferator-activated receptor-gamma (PPAR-γ), has been demonstrated to have anti-inflammatory actions. In this study, we investigated whether 15d-PGJ2 as a PPAR-γ ligand could exert neuroprotective effects in rat pheochromocytoma (PC12) cells in PPAR-γ dependent manner. In our experiment, using PC12 cells, the levels of NF-κB, Nrf2, γ-glutamylcysteine synthetase (γ-GCS), hemeoxygenase (HO-1) and apoptosis factors were determined using Western blot in different groups. Also cell viability was determined by the conventional MTT (3-[4, 5-dimethylthiazol-2-yl]-2, 5-diphenyl tetrazolium bromide) reduction assay and two staining involved Hoechst staining and Acridine Ordange/Ethidiume Bromide staining respectively. Results: Our results show that NS-398, a selective COX-2 inhibitor and 15d-PGJ2, a natural potent ligand of PPAR-γ, were neuroprotective through modulation of at least three different, but related pathways and molecules, including NF-κB and Nrf2 signaling pathway. Our data showed that 15d-PGJ2 and NS-398 induced Nrf2 signaling pathway and its downstream factors such as HO-1 and γ-GCS, while 15d-PGJ2 and NS-398 decreased NF-κB level. Interestingly, the observed protective effects were mediated through PPAR-γ-dependent mechanisms, as they reversed by GW9662, an irreversible antagonist of PPAR-γ receptor. Discussion: Thus we conclude that 15d-PGJ2 as well as NS-398 exert anti cell death effect in a PPAR-γ dependent mechanisms. Methods:
کلیدواژههای انگلیسی مقاله
Cyclooxygenase,PPAR-γ,PC12,Nrf2,15d-PGJ2,Neuroprotective.
نویسندگان مقاله
شهناز بابایی آبراکی | shahnaz babaei abraki
پرنیان اسلامی | parnian eslami
فریبا خداقلی | fariba khodagholi
نشانی اینترنتی
http://bcn.iums.ac.ir/browse.php?a_code=A-10-1-98&slc_lang=en&sid=en
فایل مقاله
فایلی برای مقاله ذخیره نشده است
کد مقاله (doi)
زبان مقاله منتشر شده
en
موضوعات مقاله منتشر شده
Clinical Neuroscience
نوع مقاله منتشر شده
Original
برگشت به:
صفحه اول پایگاه
|
نسخه مرتبط
|
نشریه مرتبط
|
فهرست نشریات