• Long Pan, Dun-Chen Yao, Yu-Zhong Yu, Sheng-Jie Li, Bing-Jun Chen, Gui-He Hu, Chang Xi, Zi-Hui Wang, Hong-Yan Wang, Jian-Hua Li, and Yong-Sheng Tu.
• Department of Physiology, School of Basic Sciences, Guangzhou Medical University, Guangzhou 511436, China; The Third Clinical Medical College, Guangzhou Medical University, Guangzhou 511436, China.
• Biochem. Biophys. Res. Commun. 2016 Sep 30; 478 (4): 1602-8.

AbstractNecroptosis is a recently discovered necrotic cell death which is regulated by receptor interacting protein kinase 1 (RIPK1) and RIPK3 under the stimulus of death signal and can be inhibited by necrostatin-1 (Nec-1) specifically. Therefore, the aim was to investigate the role of necroptosis in a rat model of acute respiratory distress syndrome (ARDS) induced by oleic acid (OA) and assess the effect of Nec-1 on lung injury in ARDS. Our results found that RIPK1, RIPK3 and mixed lineage kinase domain-like protein (MLKL) were abundantly expressed in rat lung tissues of OA-induced ARDS. Nec-1 pretreatment improved pulmonary function and attenuated lung edema dramatically in OA-induced ARDS rats. Furthermore, Nec-1 reduced RIPK1-RIPK3 interaction and down-regulated RIPK1-RIPK3-MLKL signal pathway, and inhibited inflammatory response by reducing neutrophil infiltration and protein leakage into lung tissue in OA-induced ARDS. Collectively, our study proves the intervention of necroptosis in OA-induced ARDS. Moreover, our findings imply that Nec-1 plays an important role in the treatment of ARDS via inhibiting necroptosis and inflammation.Copyright © 2016 Elsevier Inc. All rights reserved.

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