Yamato Fumiko, Takaya Junji, Tsuji Shoji, Hasui Masafumi, Kaneko Kazunari
Department of Pediatrics, Kansai Medical University, Osaka, Moriguchi 570-8506, Japan.
ISRN Inflamm. 2012 Dec 4;2012:347852. doi: 10.5402/2012/347852. eCollection 2012.
Background. Although angiotensin II (Ang II) has inflammatory effects, little is known about its role in polymorphonuclear leucocytes (PMLs). To elucidate the role of Ang II in PMLs ROS production, we examined hydrogen peroxide (H2O2), one of the ROS, and NO production in AT1a receptor knockout (AT1KO) mice. Methods and Results. PMLs were analyzed from Ang II type 1a receptor knockout mice (AT1KO) and C57BL/6 wild type mice. Using flow cytometry, we studied hydrogen peroxide (H2O2) production from PMLs after Staphylococcus aureus phagocytosis or phorbol myristate acetate (PMA) stimulation. Nitric oxide (NO) production in the AT1KO was low at basal and after phagocytosis. In the AT1KO, basal H2O2 production was low. After PMA or phagocytosis stimulation, however, H2O2 production was comparable to wild type mice. Next we studied the H2O2 production in C57BL/6 mice exposed to Ang II or saline. H2O2 production stimulated by PMA or phagocytosis did not differ between the two groups. Conclusions. AT1a pathway is not necessary for PMLs H2O2 production but for NO production. There was a compensatory pathway for H2O2 production other than the AT1a receptor.
背景。尽管血管紧张素II（Ang II）具有炎症作用，但其在多形核白细胞（PMLs）中的作用却鲜为人知。为了阐明Ang II在PMLs产生活性氧（ROS）中的作用，我们检测了AT1a受体基因敲除（AT1KO）小鼠中ROS之一的过氧化氢（H2O2）以及一氧化氮（NO）的产生情况。方法与结果。从血管紧张素II 1a型受体基因敲除小鼠（AT1KO）和C57BL/6野生型小鼠中分析PMLs。使用流式细胞术，我们研究了金黄色葡萄球菌吞噬或佛波酯（PMA）刺激后PMLs产生过氧化氢（H2O2）的情况。AT1KO小鼠在基础状态和吞噬后一氧化氮（NO）的产生量较低。在AT1KO小鼠中，基础过氧化氢（H2O2）产生量较低。然而，在PMA或吞噬刺激后，过氧化氢（H2O2）的产生量与野生型小鼠相当。接下来，我们研究了暴露于Ang II或生理盐水的C57BL/6小鼠中过氧化氢（H2O2）的产生情况。两组之间PMA或吞噬刺激引起的过氧化氢（H2O2）产生量没有差异。结论。AT1a途径对于PMLs产生过氧化氢（H2O2）不是必需的，但对于产生一氧化氮（NO）是必需的。除了AT1a受体外，存在一条过氧化氢（H2O2）产生的代偿途径。
