Propofol prevents human umbilical vein endothelial cell injury from Ang II-induced apoptosis by activating the ACE2-(1-7)-Mas axis and eNOS phosphorylation.
Propofol prevents human umbilical vein endothelial cell injury from Ang II-induced apoptosis by activating the ACE2-(1-7)-Mas axis and eNOS phosphorylation.
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异丙酚通过激活 ACE2-(1-7)-Mas 轴和 eNOS 磷酸化防止 Ang II 诱导的细胞凋亡损伤人脐静脉内皮细胞
DOI：
10.1371/journal.pone.0199373
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发表时间：
2018
期刊：
影响因子：
3.7
通讯作者：
Hu Z
中科院分区：
文献类型：
--
作者：
Zhang L;Wang J;Liang J;Feng D;Deng F;Yang Y;Lu Y;Hu Z
血管紧张素II（AngII）是一种血管活性肽，可引起动脉血压升高，导致高血压，并可直接诱导血管内皮细胞凋亡。最近的研究表明，异丙酚预处理减弱血管紧张素II诱导的人冠状动脉内皮细胞凋亡。然而，其基本机制在很大程度上仍然未知。在这里，我们研究了在存在或不存在异丙酚治疗的情况下，血管紧张素II诱导的人脐静脉内皮细胞（HUVEC）细胞凋亡，发现异丙酚以剂量依赖性方式减弱血管紧张素II诱导的细胞凋亡。此外，酶联免疫吸附试验（ELISA）显示，丙泊酚治疗后，血管紧张素（1-7）（Ang（1-7））与Ang II的比例增加。我们检测了ACE 2、Ang（1-7）和Mas的表达，发现ACE 2-Ang（1-7）-Mas轴被丙泊酚上调，而ACE 2过表达增加了磷酸化内皮型一氧化氮合酶（phosphorylated eNOS）的表达，siACE 2导致了内皮型一氧化氮合酶（eNOS）磷酸化的抑制。结论：丙泊酚可通过激活ACE 2-Ang（1-7）-Mas轴，上调eNOS的表达和磷酸化水平，抑制Ang Ⅱ诱导的内皮细胞凋亡。
Angiotensin II (AngII), a vasoactive peptide that elevates arterial blood pressure and results in hypertension, has been reported to directly induce vascular endothelial cell apoptosis. Recent work has demonstrated that propofol pre-treatment attenuates angiotensin II-induced apoptosis in human coronary artery endothelial cells. However, the underlying mechanism remains largely unknown. Here, we investigated human umbilical vein endothelial cells (HUVECs) subjected to angiotensin II-induced apoptosis in the presence or absence of propofol treatment and found that angiotensin II-induced apoptosis was attenuated by propofol in a dose-dependent manner. Furthermore, ELISA assays demonstrated that the ratio of angiotensin (1–7) (Ang (1–7)) to Ang II was increased after propofol treatment. We examined the expression of ACE2, Ang (1–7) and Mas and found that the ACE2-Ang (1–7)-Mas axis was up-regulated by propofol, while ACE2 overexpression increased phosphorylated endothelial nitric oxide synthase (phosphorylated eNOS) expression and siACE2 resulted in the repression of endothelial nitric oxide synthase (eNOS) phosphorylation. In conclusion, our study revealed that propofol can inhibit endothelial cell apoptosis induced by Ang II by activating the ACE2-Ang (1–7)-Mas axis and further up-regulating the expression and phosphorylation of eNOS.
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