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AVE 0991
本产品不向个人销售,仅用作科学研究,不用于任何人体实验及非科研性质的动物实验。
AVE 0991图片
包装与价格:
包装价格(元)
10mM (in 1mL DMSO)电议
2mg电议
5mg电议
10mg电议
100mg电议

产品介绍

Preparation Method

Competition experiments with increasing concentrations of AVE 0991 and unlabeled Ang-(1 7) were performed in the presence of 10 nmol/L [125I]-Ang-(1-7). Assays were terminated by vacuum filtration ( 15 mm Hg) over Durapore filters (0.65 |, Opak 96-well plates, Millipore) presoaked with 1% BSA.

Applications

AVE 0991 and unlabeled Ang-(1-7) competed the specific binding of [125I]-Ang-(1-7), with IC50 values of 21 !A35 and 220 !A 280 nmol/L, respectively (each n=3). The Ang-(1-7) analogue [D-Ala7]-Ang-(1 7) totally competed the specific binding of [125I]-Ang-(1-7), with an IC50 value of 0.41 !A3.0 |ol/L (n=3).

Cell lines

Chinese hamster ovary (CHO) cells

Preparation Method

Binding of rhodamine Ang-(1-7) in Mas-transfected CHO cells was performed under similar conditions using 2*10 -9 mol/L rhodamine-labeled Ang-(1-7) in the presence or absence of AVE 0991(10 -6 mol/L), CV11974, or PD123319

Reaction Conditions

AVE 0991 (10-6mol/L)

Applications

AVE 0991 displaced the binding of 125I-Ang-(1-7) in Mas-transfected monkey kidney cells (COS) cells (IC50=4.75x10(-8) mol/L) and of rhodamine-Ang-(1-7) in Mas-transfected Chinese hamster ovary (CHO) cells. It also produced NO release in Mas-transfected CHO cells blocked by A-779 but not by angiotensin II type-1 (AT1) and AT2 antagonists.

Animal models

Male C57BL/6J mice (8¨C10 weeks old; 24¨C26 g)

Preparation Method

Twenty-four h after ligation, the surviving mice were randomly divided into four groups: 1) sham-operated group, 2) vehicle-treated AB group (vehicle-treated group ), 3) AB mice treated with AVE 0991 ( AVE 0991 group ). AVE 0991 group was administered orally once a day at AVE 0991 (20 mg kg/day) for 4 weeks while isovolumic sodium chloride was administrated in the same manner for the sham-operated and vehicle-treated group.

Dosage form

AVE 0991 (20 mg kg/day) for 4 weeks

Applications

AVE 0991 treatment could attenuate cardiac hypertrophy and improve heart function, which may be due to reduce oxidative stress./p>

产品描述

AVE 0991 is a Nonpeptide Mimic of the Effects of Angiotensin-(1-7) on the Endothelium. AVE 0991 and unlabeled Ang-(1-7) competed for high-affinity binding of [125I]-Ang-(1-7) to bovine aortic endothelial cell membranes with IC50 values of 21+/-35 and 220+/-280 nM, respectively[4].

AVE 0991 displaced the binding of 125I-Ang-(1-7) in Mas-transfected monkey kidney cells (COS) cells (IC50=4.75x10(-8) mol/L) and of rhodamine-Ang-(1-7) in Mas-transfected Chinese hamster ovary (CHO) cells. It also produced NO release in Mas-transfected CHO cells blocked by A-779 but not by angiotensin II type-1 (AT1) and AT2 antagonists[7].

AVE 0991 attenuates oxidative stress and neuronal apoptosis via Mice were underwent aortic banding to induce cardiac hypertrophy followed by the administration of AVE 0991 (20 mg kg.day (-1)) for 4 weeks. It was shown that AVE 0991 reduced left ventricular hypertrophy and improved heart function, characterized by decreases in left ventricular weight and left ventricular end-diastolic diameter, and increases in ejection fraction. Moreover, AVE 0991 significantly down-regulated mean myocyte diameter and attenuate the gene expression of the hypertrophic markers[2].Mas/PKA/CREB/UCP-2 pathway after subarachnoid hemorrhage in rats[1]. Enhanced Ang II and attenuated Ang-(1-7) levels were also observed in the liver tissue of heatstroke rats, which were consistent with their receptors and converting enzymes. Hepatic damage associated with increased ROS and protein expression levels of NOX4, NLRP3, caspase-1, and IL-1β was attenuated by AVE 0991, an analogue of Ang-(1-7)[3]. Oral treatment with AVE 0991 reduces blood-pressure cardiac remodeling and improves baroreflex sensitivity in 2K1C renovascular hypertensive rats[5]. AVE 0991 prevented AngII-inducing myocardial hypertrophy in a dose-dependent fashion, a process that may be associated with the inhibition of TGF-beta1/Smad2 signaling[6].

References:
[1]. Mo J, Enkhjargal B, et,al. AVE 0991 attenuates oxidative stress and neuronal apoptosis via Mas/PKA/CREB/UCP-2 pathway after subarachnoid hemorrhage in rats. Redox Biol. 2019 Jan;20:75-86. doi: 10.1016/j.redox.2018.09.022. Epub 2018 Sep 28. PMID: 30296700; PMCID: PMC6174866.
[2]. Ma Y, Huang H, et,al. AVE 0991 attenuates cardiac hypertrophy through reducing oxidative stress. Biochem Biophys Res Commun. 2016 Jun 10;474(4):621-625. doi: 10.1016/j.bbrc.2015.09.050. Epub 2015 Sep 25. PMID: 26403967.
[3]. Zhang M, Zhu X, et,al. AVE 0991 Attenuates Pyroptosis and Liver Damage after Heatstroke by Inhibiting the ROS-NLRP3 Inflammatory Signalling Pathway. Biomed Res Int. 2019 Aug 19;2019:1806234. doi: 10.1155/2019/1806234. PMID: 31531346; PMCID: PMC6720052.
[4]. Wiemer G, Dobrucki LW, et,al. AVE 0991, a nonpeptide mimic of the effects of angiotensin-(1-7) on the endothelium. Hypertension. 2002 Dec;40(6):847-52. doi: 10.1161/01.hyp.0000037979.53963.8f. PMID: 12468568.
[5]. Cunha TM, Lima WG, et,al.The nonpeptide ANG-(1-7) mimic AVE 0991 attenuates cardiac remodeling and improves baroreflex sensitivity in renovascular hypertensive rats. Life Sci. 2013 Mar 12;92(4-5):266-75. doi: 10.1016/j.lfs.2012.12.008. Epub 2013 Jan 16. PMID: 23333828.
[6]. He JG, Chen SL, et,al. The nonpeptide AVE0991 attenuates myocardial hypertrophy as induced by angiotensin II through downregulation of transforming growth factor-beta1/Smad2 expression. Heart Vessels. 2010 Sep;25(5):438-43. doi: 10.1007/s00380-009-1213-7. Epub 2010 Jul 31. PMID: 20676968.
[7]. Pinheiro SV, SimÕes e Silva AC, et,al. Nonpeptide AVE 0991 is an angiotensin-(1-7) receptor Mas agonist in the mouse kidney. Hypertension. 2004 Oct;44(4):490-6. doi: 10.1161/01.HYP.0000141438.64887.42. Epub 2004 Aug 23. PMID: 15326087.