کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5949798 | 1172392 | 2011 | 8 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Compound C independent of AMPK inhibits ICAM-1 and VCAM-1 expression in inflammatory stimulants-activated endothelial cells in vitro and in vivo
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کلمات کلیدی
NF-κBVCAM-1HUVECiNOSICAM-1AICARAMPKPI3KMAPK - MAPKinflammation - التهاب( توروم) compound C - ترکیب Ctumor necrosis factor-alpha - تومور نکروز عامل آلفاHuman umbilical vein endothelial cells - سلول های اندوتلیالی ورید ناف انسانEndothelial cells - سلولهای اندوتلیالinducible nitric oxide synthase - سنتاز اکسید نیتریک القاییTNF-α - فاکتور نکروز توموری آلفاnuclear factor kappa-B - فاکتور هسته ای کاپا-Bintracellular adhesion molecule-1 - مولکول چسبندگی داخل سلولی -1vascular cell adhesion molecule-1 - مولکول چسبندگی سلولی عروقی-1Adhesion molecules - مولکولهای چسبندگیmitogen activated protein kinase - پروتئین کیناز فعال Mitogen فعال استadenosine monophosphate-activated protein kinase - پروتئین کیناز فعال شده با آدنوزین مونوفسفات
موضوعات مرتبط
علوم پزشکی و سلامت
پزشکی و دندانپزشکی
کاردیولوژی و پزشکی قلب و عروق
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چکیده انگلیسی
Activation of the NF-κB and mitogen activated protein (MAP) kinases plays an important role in the expression of inflammatory genes such as adhesion molecules. Although compound C is known as an AMPK inhibitor, AMPK-independent action of it has been recognized. Effects on the expression of ICAM-1 and VCAM-1 by compound C were investigated in TNF-α-activated human umbilical vein endothelial cells (HUVECs) in vitro and in thoracic aorta of rats treated with lipopolysaccharide (LPS) in vivo. Compound C inhibited ICAM-1 and VCAM-1 expression at the transcriptional as well as translational level in TNF-α-activated HUVECs. In both DN-AMPK- and AMPKα1-siRNA-transfected HUVECs, compound C still inhibited TNF-α-induced VCAM-1 and ICAM-1 expression, indicating that this is AMPK-independent action. Interestingly, compound C significantly inhibited NF-κB activity and translocation of p65 to nucleus in HUVECs when activated with TNF-α. Importantly, administration of compound C (0.2 mg/kg) significantly reduced expression of both ICAM-1 and VCAM-1 in LPS-treated rat thoracic aortas. In addition, compound C significantly inhibited iNOS and production of NO in both TNF-α- and LPS-activated RAW 264.7 cells. Finally, compound C significantly inhibited phosphorylation of Akt and p-38MAPK but not protein kinase c or ERK1/2 in HUVECs. Taken together, we conclude that adhesion molecules (ICAM-1, VCAM-1) are to be the novel targets of compound C in preventing inflammatory insult to endothelial cells independent of AMPK inhibition via inhibition of NF-κB activity along with inhibition of phosphorylation of PI3K and P38 MAPK.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Atherosclerosis - Volume 219, Issue 1, November 2011, Pages 57-64
Journal: Atherosclerosis - Volume 219, Issue 1, November 2011, Pages 57-64
نویسندگان
Young Min Kim, Min Young Kim, Hye Jung Kim, Gu Seob Roh, Gyung Hyuck Ko, Han Geuk Seo, Jae Heun Lee, Ki Churl Chang,