Selected article for: "ace expression and lung expression"
Author: Yan, Xiujuan; Li, Yingxiu; Choi, Yun Ho; Wang, Chongyang; Piao, Yihua; Ye, Jing; Jiang, Jingzhi; Li, Liangchang; Xu, Huixian; Cui, Qingsong; Yan, Guanghai; Jin, Minggen
Title: Protective Effect and Mechanism of Alprostadil in Acute Respiratory Distress Syndrome Induced by Oleic Acid in Rats
  • Document date: 2018_10_8
    • ID: 7ea7ur3b_32
    Snippet: In this study, we demonstrated that OA administration evoked severe lung injury, which was characterized by increased inflammatory cell infiltration, edema, and hemorrhage in the interstitium and alveolus, as well as collagen deposition. In addition, OA administration significantly increased lung W/D ration, the expression of ACE, pro-inflammatory factors, pro-apoptotic proteins, and activation of MAPKs and NF-kB signaling pathways in the rat lun.....
    Document: In this study, we demonstrated that OA administration evoked severe lung injury, which was characterized by increased inflammatory cell infiltration, edema, and hemorrhage in the interstitium and alveolus, as well as collagen deposition. In addition, OA administration significantly increased lung W/D ration, the expression of ACE, pro-inflammatory factors, pro-apoptotic proteins, and activation of MAPKs and NF-kB signaling pathways in the rat lung tissue. Importantly, alprostadil treatment significantly attenuated OA-induced ARDS symptoms, as well as suppressing the elevation of these ARDS-related proteins and activation of the MAPKs and NF-kB pathways. Taken together, these findings suggest that alprostadil administration prevents OA-induced ARDS and inflammation and may be useful as a therapeutic agent for ARDS treatment.

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