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

Alprostadil ameliorates OA-induced lung tissue histopathological changes Next, we investigated the effect of Alprostadil on the histopathological changes of lungs by H&E staining. The structure of the alveoli was complete and there was no obvious pathological change in the control group (Figure 2A ). OA challenge caused significant pathological changes, including infiltration of inflammatory cells, aggregation of neutrophils in the alveolus and alveolar fluid, thickening of the alveolar wall, and pulmonary congestion (Figure 2A ). Alprostadil treatment ameliorated the tissue damage in a dose-dependent manner. Importantly, in the OA + Alprostadil (10 μg/kg) group, the damaged structure of the alveoli was obviously restored compared with that in the OA model group. Moreover, the lung injury scores ( Figure 2B ) of the OA model group were significantly increased as compared with the control group. In contrast, compared with the OA model group, alprostadil significantly decreased the lung injury score. Similar results were obtained by Masson trichrome staining. As shown in Figure 3 , more collagen deposition and higher fibrosis scores were observed in OA model group compared with the control group. Alprostadil treatment reduced collagen deposition and fibrosis scoring in a dose-dependent manner. These data suggest that Alprostadil protects rat from OA-induced lung tissue damage.