Angiotensin(1-7)(acetate)

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包装与价格：

包装	价格(元)
10mM (in 1mL DMSO)	询价
2mg	询价
5mg	询价
10mg	询价
25mg	询价
50mg	询价
100mg	询价

Angiotensin1-7(Ang-(1-7))acetate是肾素-血管紧张素系统(RAS)中的一种内源性七肽，由于其在心肌细胞中的抗炎和抗纤维化活性而具有心脏保护作用。Angiotensin1-7acetate抑制纯化的犬血管紧张素转换酶(ACE)活性(IC50=0.65μM)。Angiotensin1-7acetate通过抑制血管紧张素转换酶和释放一氧化氮作为激肽诱导的血管舒张的局部协同调节剂。Angiotensin1-7acetate阻断血管紧张素Ⅱ诱导的平滑肌细胞增殖和肥大，对内皮细胞具有抗血管生成和生长抑制作用。

别名	Ang-(1-7) (acetate)
分子式	C₄₃H₆₆N₁₂O₁₃
分子量	959.06
溶解度	Water: 125 mg/mL (130.34 mM)
储存条件	Store at -20℃
General tips	For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.
Shipping Condition	Evaluation sample solution : ship with blue ice All other available size: ship with RT , or blue ice upon request
产品描述	Angiotensin 1-7 (Ang-(1-7)) acetate is an endogenous heptapeptide from the renin-angiotensin system (RAS) with a cardioprotective role due to its anti-inflammatory and anti-fibrotic activities in cardiac cells. Angiotensin 1-7 acetate inhibits purified canine ACE activity (IC50=0.65 μM). Angiotensin 1-7 acetate acts as a local synergistic modulator of kinin-induced vasodilation by inhibiting ACE and releasing nitric oxide. Angiotensin 1-7 acetate blocks Ang II-induced smooth muscle cell proliferation and hypertrophy and shows antiangiogenic and growth-inhibitory effects on the endothelium[1][2][3]. Angiotensin 1-7 (Ang-(1-7)) inhibits cultured vascular smooth muscle cell growth, whereas equal molar concentration of Ang II stimulates cell growth[2].Angiotensin 1-7 (Ang 1-7) abrogates the methylglyoxal-modified albumin (MGA)-stimulated myofibroblast phenotype by inhibiting the chronic stimulation of the TGF-β-ERK pathway in NRK-52E cells[4].Angiotensin 1-7 signals through the Mas receptor ( MasR) in opposition to Ang II/angiotensin II type 1 receptor (AT1R), promoting anti-inflammatory,vasodilatory, and neuroprotective effects[5]. Daily Angiotensin 1-7 (Ang-(1-7)) treatment (0.01-0.06 mg/kg) results in significant amelioration of DSS-induced colitis. Colitis-associated phosphorylation of p38, ERK1/2 and Akt is reduced by Ang 1-7 treatment[3]. [1]. GÓmez-Mendoza DP, et al. Angiotensin-(1-7) oral treatment after experimental myocardial infarction leads to downregulation of CXCR4. J Proteomics. 2019;208:103486. [2]. Li P, et al. Angiotensin-(1-7) augments bradykinin-induced vasodilation by competing with ACE and releasing nitric oxide. Hypertension. 1997 Jan;29(1 Pt 2):394-400. [3]. Khajah MA, et al. Anti-Inflammatory Action of Angiotensin 1-7 in Experimental Colitis. PLoS One. 2016 Mar 10;11(3):e0150861. [4]. Alzayadneh EM, et al. Angiotensin-(1-7) abolishes AGE-induced cellular hypertrophy and myofibroblast transformation via inhibition of ERK1/2. Cell Signal. 2014 Sep 19. pii: S0898-6568(14)00314-3. [5]. Janatpour ZC, et al. Subcutaneous Administration of Angiotensin-(1-7) Improves Recovery after Traumatic Brain Injury in Mice. J Neurotrauma. 2019;36(22):3115-3131.