Lipoxin A4 Ameliorates Acute Pancreatitis-Associated Acute Lung Injury through the Antioxidative and Anti-Inflammatory Effects of the Nrf2 Pathway

Figure 3

LXA4 alleviated TNF-α-induced damage and inhibited ROS generation in vitro. TNF-α has been commonly used for AP-ALI experimental modeling in vitro, and we used the concentration established in our previous study. HPMECs were pretreated with 50 ng/ml LXA4 for 1 h, followed by stimulation with 50 ng/ml TNF-α for 24 h. (a–c) Fold changes in the mRNA expression of IL-1β, IL-6, and E-selectin in HPMECs were calculated. The mRNA levels of IL-1β, IL-6, and E-selectin were measured by RT-PCR. (d) Cellular ROS were observed by fluorescence microscopy. (e) The quantitative mean fluorescence intensity in each treatment group is shown. (f) The levels of ROS were determined by flow cytometric analysis. (g) Flow cytometric analysis results are presented as a histogram. and vs. the control group. ^# and ^## vs. the TNF-α group. TNF-α: the TNF-α group; TNF-α+LXA4: the TNF-α+Lipoxin A4 group; ROS: reactive oxygen species; AP-ALI: the acute pancreatitis-induced acute lung injury; HPMECs: human pulmonary microvascular endothelial cells.

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