Angiotensin-converting enzyme 2 attenuates inflammatory response and oxidative stress in hyperoxic lung injury by regulating NF-κB and Nrf2 pathways

QJM : Monthly Journal of the Association of Physicians
Yue FangZhenwei Liu

Abstract

To investigate the role of angiotensin-converting enzyme 2 (ACE2) in hyperoxic lung injury. Adult mice were exposed to 95% O2 for 72 h to induce hyperoxic lung injury, and simultaneously treated with ACE2 agonist diminazene aceturate (DIZE) or inhibitor MLN-4760. ACE2 expression/activity in lung tissue and Ang(1-7)/AngⅡin BALF, and the severity of hyperoxic lung injury was evaluated. The levels of inflammatory factors in BALF and lung tissue and the expression levels of phospho-p65, p65, and IkBα were measured. Oxidative parameter and antioxidant enzyme levels in lung tissue were measured to assess oxidative stress. Finally, the expression levels of Nrf2, NQO1, and HO-1 were measured using Western blotting. Hyperoxia treatment significantly decreased lung ACE2 expression/activity and increased the Ang II/Ang-(1-7) ratio, while co-treatment with hyperoxia and DIZE significantly increased lung ACE2 expression/activity and decreased the Ang II/Ang-(1-7) ratio. By contrast, co-treatment with hyperoxia and MLN-4760 significantly decreased lung ACE2 expression/activity and increased the Ang II/Ang-(1-7) ratio. Hyperoxia treatment induced significant lung injury, inflammatory response, and oxidative stress, which were attenuated by DI...Continue Reading

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Citations

Apr 29, 2020·European Journal of Preventive Cardiology·Xiaofeng Dai
Jun 9, 2020·Clinical Science·Katharina LanzaAna Cristina Simões E Silva
Jun 9, 2020·Clinical and Translational Medicine·Liyang LiXiangdong Wang
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