کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10956255 | 1098814 | 2012 | 12 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Olmesartan attenuates the development of heart failure after experimental autoimmune myocarditis in rats through the modulation of ANG 1-7 mas receptor
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کلمات کلیدی
PI3KLVEDPLVPc-Jun-N-terminal kinaseMAPKAPK-2LVDdAT2RAT1RLVDsRIAMAPK signaling pathwaysACE-2RASangiotensin-II type 1 receptorradio-immuno assayJnkARBs - ARB هاMAPK - MAPKEAM - POMAngiotensin 1–7 - آنژیوتانسین 1-7angiotensin-II - آنژیوتانسین IIAngiotensin-(1-7) - آنژیوتانسین- (1-7)Olmesartan - اولسمارکتانNADPH oxidase - اکسیداز NADPH ELISA - تست الیزاEnzyme-linked immunosorbent assay - تست الیزاAng-II - دومdihydroethidium - دی هیدروتیدیمrenin-angiotensin system - سیستم رنین-آنژیوتانسینphosphatidylinositol-3-kinase - فسفاتیدیلینواستیل-3-کینازleft ventricular pressure - فشار بطن چپAngiotensin receptor blockers - مسدود کننده های گیرنده آنژیوتانسینexperimental autoimmune myocarditis - میوکاردیت خود ایمنی تجربیnicotinamide adenine dinucleotide phosphate oxidase - نیکوتین آمید آدنین دیونوکلئوتید فسفات اکسیدازDHE - وmitogen-activated protein kinase - پروتئین کیناز فعال با mitogen
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
بیولوژی سلول
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چکیده انگلیسی
Angiotensin-converting enzyme 2 (ACE-2) is a membrane-associated carboxy-peptidase catalyzes the conversion of the vasoconstrictor angiotensin (ANG)-II to the vasodilatory peptide ANG 1-7. In view of the expanding axis of the renin angiotensin system, we have investigated the cardioprotective effects of olmesartan (10Â mg/kg/day) in experimental autoimmune myocarditis. Olmesartan treatment effectively suppressed the myocardial protein expressions of inflammatory markers in comparison to the vehicle-treated rats. However, the protein and mRNA levels of ACE-2 and ANG 1-7, and its receptor Mas were upregulated in olmesartan treated group compared to vehicle-treated rats. Olmesartan medoxomil treatment significantly decreased the expression levels of phospho-p38 mitogen-activated protein kinase (MAPK), phospho-JNK, phospho-ERK and phospho-(MAPK) activated protein kinase-2 than with those of vehicle-treated rats. Moreover, vehicle-treated rats were shown to be up-regulated protein expressions of NADPH oxidase subunits (p47phox, p67phox and Nox-4), myocardial apoptotic markers and endoplasmic reticulum stress markers in comparison to those of normal and all these effects are expectedly down-regulated by an olmesartan. In addition, attenuated protein levels of phosphatidylinositol-3-kinase (PI3K) and phospho-Akt in the vehicle-treated EAM rats were prevented by olmesartan treatment. Our results suggest that beneficial effects of olmesartan treatment was more effective therapy in combating the inflammation, oxidative stress, apoptosis and signaling pathways associated with heart failure at least in part via the modulation of ANG 1-7 mas receptor.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Molecular and Cellular Endocrinology - Volume 351, Issue 2, 4 April 2012, Pages 208-219
Journal: Molecular and Cellular Endocrinology - Volume 351, Issue 2, 4 April 2012, Pages 208-219
نویسندگان
Vijayakumar Sukumaran, Punniyakoti T. Veeraveedu, Narasimman Gurusamy, Arun Prasath Lakshmanan, Ken'ichi Yamaguchi, Meilei Ma, Kenji Suzuki, Masaki Nagata, Ritsuo Takagi, Makoto Kodama, Kenichi Watanabe,