Protective Effect and Mechanism of Alprostadil in Acute Respiratory Distress Syndrome Induced by Oleic Acid in Rats

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

Western blot analysis showed that phosphorylation of MAPKs was significantly up-regulated by OA, including p-p38 MAPK ( Figure 5A , 5B), p-ERK1/2 ( Figure 5A , 5C), and p-JNK ( Figure 5A, 5D) . Moreover, OA administration markedly increased the phosphorylation of p65 ( Figure 5A, 5E) conditions. It has been confirmed that serum ACE activity is significantly elevated in active ARDS patients, and that the measurement of serum ACE activity is useful in following the clinical course of the disease [39] . Several studies have suggested that monitoring serum ACE is useful as an indicator of endothelial cell integrity [40] . Staining results showed that the expression of ACE protein in the lung tissue from the OA model group was obviously higher than that from the control group ( Figure 7A ), suggesting that ACE is involved in the development of ARDS. In contrast, in the OA + Alprostadil (5 and 10 μg/kg) group, the expression of ACE was partially reduced compared with that in the OA model group (Figure 7A, 7B) .