Selected article for: "activation pathway and lung injury"
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_3
    Snippet: A recent study showed that activation of the mitogen-activated protein kinases (MAPKs) pathway is involved in ARDS [11] . The phosphorylation levels of p38 MAPK, extracellular signal-regulated kinase (ERK), and Jun N-terminal kinase (JNK) are all significantly increased in LPS-induced lung injury [12] . Consequently, inhibition of these proteins efficiently attenuates LPS-induced pulmonary inflammatory response [13, 14] . Additionally, the possib.....
    Document: A recent study showed that activation of the mitogen-activated protein kinases (MAPKs) pathway is involved in ARDS [11] . The phosphorylation levels of p38 MAPK, extracellular signal-regulated kinase (ERK), and Jun N-terminal kinase (JNK) are all significantly increased in LPS-induced lung injury [12] . Consequently, inhibition of these proteins efficiently attenuates LPS-induced pulmonary inflammatory response [13, 14] . Additionally, the possible mechanism by which oleic acid (OA) induces acute lung injury (ALI)/ARDS in rats is that OA activates the NF-kB signaling pathway to increase the expressions of many pro-inflammatory cytokines, including TNF-a and IL-1b [15] . Therefore, we hypothesized that alprostadil can protect against OA-induced ARDS by inhibiting the MAPKs and NF-kB pathways.

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