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\u003C0.01)。血管紧张素(1-7)具有与Ang II不同的新型生物学功能。与Ang II相反,血管紧张素(1-7)不是二倍体或醛固酮促分泌素,但与Ang II类似,它刺激血管加压素,前列腺素和NO的释放。血管紧张素(1-7)抵消Ang II的几种作用。在犬冠状动脉和猪冠状动脉中,血管紧张素(1-7)引起血管舒张,而Ang II则分叉地收缩冠状动脉。血管紧张素(1-7)抑制培养的血管平滑肌细胞生长,而等摩尔浓度的Ang II刺激细胞生长[1]。血管紧张素1-7(Ang 1-7)通过抑制NRK-52E细胞中TGF-β-ERK途径的慢性刺激来消除甲基乙二醛修饰的白蛋白(MGA)刺激的肌成纤维细胞表型[2]。",{"key":234,"value":235},"体内研究","在结肠炎诱导后第7天,与未处理(UT)组相比,在硫酸葡聚糖钠(DSS)处理的小鼠中证实血管紧张素1-7(Ang 1-7)的血浆水平降低7倍。另一方面,与UT小鼠(0.04ng\u002FmL)相比,在第7天(0.09ng\u002FmL)DSS处理的小鼠的结肠匀浆中观察到Ang 1-7的显着增加[3]。卵巢切除的(OV)雌性Wistar-大鼠接受雌二醇(500μg\u002F kg \u002F周)或载体两周。对动物进行麻醉,插管,并将反应包括平均动脉压,肾血流量(RBF)和肾血管阻力在恒定的肾灌注压水平下分级输注血管紧张素1-7(Ang 1-7)0在用OV或OV雌二醇处理的(OVE)大鼠中测定100和300ng\u002Fkg\u002Fmin,用载体或MasR拮抗剂处理; A779。对载体(Pdose \u003C0.001)和A779处理的(Pdose \u003C0.01)动物剂量依赖性地对Ang 1-7输注的RBF应答增加。然而,当MasR阻断时,与OVE大鼠相比,OV动物对Ang 1-7的RBF反应显着增加(P \u003C0.05)。当雌二醇被卵巢切除术限制时,A779增加RBF对血管紧张素(1-7)给药的反应,而这种反应在OVE动物中减弱[4]。",{"key":237,"value":238},"激酶实验","使用固定浓度的底物Hip-His-Leu（1mM）测定使用纯化犬ACE的竞争测定，并改变竞争剂[赖诺普利（0.1至100nM），血管紧张素（1-7）（10nM）的浓度。至10μM）或Sar1，Thr8-Ang II（10nM至10μM）]。抑制常数（IC 50）由各自的竞争曲线确定。为了研究血管紧张素（1-7）对完整冠状环中BK代谢的影响，将125I- [Tyr0] -BK（终浓度为1nM）加入含有三个环的管中，所述三个环用1mL Krebs缓冲液预孵育并充气在37°C下使用95％O2和5％CO2。在添加放射性标记的BK之前10分钟将赖诺普利（2μM），血管紧张素（1-7）（2μM）或Krebs'缓冲液作为对照加入到环中。在5,10和20分钟取出孵育培养基的等分试样并用1％HFBA稀释以抑制肽酶活性[1]。",{"key":240,"value":241},"细胞实验","将500μM甲基乙二醛与溶解在磷酸盐缓冲盐水（PBS）中的100μMABA温育24小时，然后在10kDa过滤器上洗涤以除去过量的甲基乙二醛，用DMEM \u002F F12无血清培养基重构并通过0.2μmicron过滤器。制备TGF-β（5ng \u002F mL）以处理实验子集中的细胞。细胞与以下一种或组合共同治疗：血管紧张素（1-7）（100 nM），D-Ala7-Ang-（1-7）（10μM），ERK1 \u002F 2激酶抑制剂，PD 98059（1 μM），TGF-β受体激酶抑制剂; SB525334（1μM），AT1受体拮抗剂氯沙坦（1μM），肾素抑制剂Aliskerin（1μM）和ACE抑制剂赖诺普利（1μM）[2]。",{"key":243,"value":244},"动物实验","小鼠[3]使用雄性和雌性BALB \u002F c小鼠（1：1比例，6-10周龄，平均体重20g）。将血管紧张素片段1-7乙酸盐水合物（Ang 1-7）以1mg \u002F mL溶解于0.9％盐水（载体）中并储存在-80℃。从实验的每一天新鲜制备各种剂量（0.01,0.06,0.1,0.3和1mg \u002F kg），并通过每次腹膜内（ip）注射以每次注射500μL的体积给予小鼠，在（预防性接近）之前或之后（治疗方法）DSS治疗。将A779（MAS-1R拮抗剂）类似地溶解在1mg \u002F mL的蒸馏水中并储存在-80℃。通过每日腹膜内注射500μL每天（持续4天）以及结肠炎诱导（预防性方法），向第二组小鼠施用新制备的1mg \u002F kg剂量。第三组小鼠接受含有水的DSS和每日ip注射0.9％盐水（载体）。第四组接受含有水的DSS以及每日腹膜内注射地塞米松（DEX），剂量为0.01-1.0mg \u002F kg或其载体（0.9％盐水）（预防方法）。大鼠[4]使用重量为200±20g的26只卵巢切除的雌性Wistar大鼠。在拮抗剂\u002F盐水输注后，通过微量注射泵以100和300ng \u002F kg \u002F min的两种不同连续剂量静脉内施用血管紧张素（1-7）。每次剂量输注15分钟;在血管紧张素（1-7）输注期间记录MAP，RPP和RBF，并且每个剂量的最后3-5分钟测量为“对血管紧张素（1-7）输注的响应”。在血管紧张素（1-7）输注期间，RPP通过可调节的主动脉钳维持在Ang1-7前输注水平。在实验结束时，通过过量麻醉剂人体杀死大鼠，取出左肾并立即称重。",{"key":246,"value":247},"参考文献","[1].\nLi 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.\n[2].\nAlzayadneh EM, et al. Angiotensin-(1-7) abolishes AGE-induced cellular hypertrophy and myofibroblast transformation via inhibition of ERK1\u002F2. Cell Signal. 2014 Sep 19. pii: S0898-6568(14)00314-3.\n[3].\nKhajah MA, et al. Anti-Inflammatory Action of Angiotensin 1-7 in Experimental Colitis. PLoS One. 2016 Mar 10;11(3):e0150861.\n[4].\nSaberi S, et al. Role of Mas receptor in renal blood flow response to angiotensin-(1-7) in ovariectomized estradiol treated rats. 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