Selected article for: "control group and lung tissue 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_28
    Snippet: The effect of alprostadil on the production of the pro-inflammatory mediators TNF-a and IL-1ß was also analyzed by Western blot at 3 h after administration of OA. OA administration caused a significant increase in TNFa and IL-1b expression in the lung tissues when compared with the control group ( Figure 4A-4C; p<0 .05). Alprostadil (2.5, 5, and 10 μg/kg) administration caused an obviously decrease in the expression of TNF-a and IL-1b in the lu.....
    Document: The effect of alprostadil on the production of the pro-inflammatory mediators TNF-a and IL-1ß was also analyzed by Western blot at 3 h after administration of OA. OA administration caused a significant increase in TNFa and IL-1b expression in the lung tissues when compared with the control group ( Figure 4A-4C; p<0 .05). Alprostadil (2.5, 5, and 10 μg/kg) administration caused an obviously decrease in the expression of TNF-a and IL-1b in the lung tissue when compared with the OA model group. These results indicate that alprostadil inhibits the production of pro-inflammatory mediators and protects rats from OA-induced lung inflammation. Alprostadil suppresses MAPKs and NF-kB signaling pathways in OA-induced ARDS rats NF-kB and MAPK signaling pathways play key roles in OAinduced ARDS pathogenesis [36, 37] ; therefore, we investigated whether alprostadil could affect these pathways.

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