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首页> 外文期刊>Apoptosis >Acetylcholine prevents angiotensin II-induced oxidative stress and apoptosis in H9c2 cells
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Acetylcholine prevents angiotensin II-induced oxidative stress and apoptosis in H9c2 cells

机译：乙酰胆碱可预防血管紧张素II诱导的H9c2细胞氧化应激和细胞凋亡

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摘要

Apoptosis of cardiomyocytes plays an important role in the development of cardiovascular diseases (CVD). Numerous studies have shown that generation of reactive oxygen species (ROS) induced by the renin-angiotensin system (RAS) is involved in this pathological process. Recent studies also suggested that acetylcholine (ACh) prevented the hypoxia-induced apoptosis of mouse ES cells by inhibiting the ROS production. However, whether ACh can inhibit the action of angiotensin II (Ang II) and subsequently prevent CVD development remains unclear. In this study, H9c2 cells were stimulated by 10−6 M Ang II for 24 h with or without 10−5 M ACh, 10−5 M ACh + 10−4 M atropine respectively. The results demonstrated that Ang II increased apoptosis index by fourfold (vs. the control group, P < 0.01), which were significantly diminished by ACh. However, the atropine (ACh receptor [AChR] inhibitor) treatment blocked the protective effect of ACh. Subsequently, Ang II significantly increases the expression and activity of NADPH oxidase so that ROS production is increased by sevenfold (vs. control group, P < 0.01). The activity and expression of caspase-3 along with the Bax/Bcl2 ratio and the levels of p38 mitogen activated protein kinase (MAPK) phosphorylation also appeared to follow a similar trend. Furthermore, we observed that ACh could reduce up-regulation of AT1 receptor expression induced by Ang II. However, all these effects of ACh were inhibited by atropine. In conclusion, ACh prevents Ang II-induced H9c2 cells apoptosis through down-regulation of the AT1 receptor and inhibition of ROS-mediated p38 MAPK activation as well as regulation of Bcl-2, Bax and caspase-3.
机译：心肌细胞的凋亡在心血管疾病（CVD）的发展中起着重要作用。大量研究表明，由肾素-血管紧张素系统（RAS）诱导的活性氧（ROS）的产生与该病理过程有关。最近的研究还表明，乙酰胆碱（ACh）通过抑制ROS的产生来防止缺氧诱导的小鼠ES细胞凋亡。但是，乙酰胆碱酯是否可以抑制血管紧张素II（Ang II）的作用并随后阻止CVD的发展尚不清楚。在这项研究中，在有或没有10 -5 M ACh，10 −5 M Ang II刺激H9c2细胞24小时。 > M ACh + 10 −4 阿托品。结果表明，Ang II使细胞凋亡指数增加了四倍（与对照组相比，P <0.01），而ACh明显降低了该指数。但是，阿托品（ACh受体[AChR]抑制剂）治疗会阻断ACh的保护作用。随后，Ang II显着增加了NADPH氧化酶的表达和活性，从而使ROS的产量增加了7倍（与对照组相比，P <0.01）。 caspase-3的活性和表达以及Bax / Bcl2比和p38丝裂原活化蛋白激酶（MAPK）磷酸化的水平也似乎遵循类似的趋势。此外，我们观察到ACh可以减少Ang II诱导的AT1受体表达的上调。但是，ACh抑制了ACh的所有这些作用。总之，ACh通过下调AT1受体和抑制ROS介导的p38 MAPK活化以及调节Bcl-2，Bax和caspase-3来防止Ang II诱导的H9c2细胞凋亡。

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