Angiotensin (1-7) (acetate) (Synonyms: Ang-(1-7) (acetate)) |
| カタログ番号GC61496 |
アンジオテンシン 1-7 (Ang-(1-7)) アセテートは、心臓細胞における抗炎症および抗線維化活性による心臓保護の役割を持つ、レニン-アンジオテンシン系 (RAS) からの内因性ヘプタペプチドです。
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Cas No.: 2855063-75-9
Sample solution is provided at 25 µL, 10mM.
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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.
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