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首页> 外文期刊>Journal of Cellular Physiology >Angiotensin-(1-7) decreases LPS-induced inflammatory response in macrophages
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Angiotensin-(1-7) decreases LPS-induced inflammatory response in macrophages

机译：血管紧张素-(1 - 7)减少LPS-induced巨噬细胞的炎症反应

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It has been previously shown that besides its classical role in blood pressure control the renin-angiotensin system, mainly by action of angiotensin II on the AT 1 receptor, exerts pro-inflammatory effects such as by inducing the production of cytokines. More recently, alternative pathways to this system were described, such as binding of angiotensin-(1-7) to receptor Mas, which was shown to counteract some of the effects evoked by activation of the angiotensin II-AT 1 receptor axis. Here, by means of different molecular approaches we investigated the role of angiotensin-(1-7) in modulating inflammatory responses triggered in mouse peritoneal macrophages. Our results show that receptor Mas transcripts were up-regulated by eightfold in LPS-induced macrophages. Interestingly, macrophage stimulation with angiotensin-(1-7), following to LPS exposure, evoked an attenuation in expression of TNF-α and IL-6 pro-inflammatory cytokines; where this event was abolished when the receptor Mas selective antagonist A779 was also included. We then used heterologous expression of the receptor Mas in HEK293T cells to search for the molecular mechanisms underlying the angiotensin-(1-7)-mediated anti-inflammatory responses by a kinase array; what suggested the involvement of the Src kinase family. In LPS-induced macrophages, this finding was corroborated using the PP2 compound, a specific Src kinase inhibitor; and also by Western blotting when we observed that Ang-(1-7) attenuated the phosphorylation levels of Lyn, a member of the Src kinase family. Our findings bring evidence for an anti-inflammatory role for angiotensin-(1-7) at the cellular level, as well as show that its probable mechanism of action includes the modulation of Src kinases activities.
机译：之前它已经表明,除了它在血压控制的经典角色肾素-血管紧张素系统,主要是通过行动的血管紧张素ⅱ1受体,产生如通过诱导促炎效应细胞因子的生产。这个系统的替代途径描述,如绑定血管紧张素- (1 - 7)受体Mas,抵消的一些效应诱发的激活血管紧张素ii受体1轴。我们研究了不同分子的方法血管紧张素-(1 - 7)在调节的作用在老鼠引发的炎症反应腹膜巨噬细胞。受体Mas成绩单都上调了8倍LPS-induced巨噬细胞。有趣的是,巨噬细胞刺激血管紧张素-(1 - 7),有限合伙人曝光后,诱发肿瘤坏死因子-α的表达和衰减il - 6促炎细胞因子;当受体Mas选择性被废除拮抗剂A779也包括在内。不同的受体Mas的表达式HEK293T细胞寻找分子机制的血管紧张素-(1 - 7)介导的抗炎通过一系列激酶反应;参与的Src激酶家族。LPS-induced巨噬细胞,这一发现证实了使用PP2化合物,一个特定的Src激酶抑制剂;吸去,当我们观察到Ang - (1 - 7)林恩的减毒的磷酸化水平Src激酶家族的成员。抗炎作用的证据血管紧张素-(1 - 7)在细胞水平上表明其可能的作用机制包括Src激酶的调制活动。

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