Objective: We aimed to investigate the regulatory mechanism of miR-133b and Sp1 in rats with severe acute pancreatitis complicated by acute lung injury.
Methods: The rats were divided into normal, NC, model, si-Sp1, miR-133b mimic, miR-133b inhibitor, and miR-133b inhibitor + si-Sp1 group and received different treatments.
Results: Compared with normal mice, model mice had a lower miR-133b expression, but higher levels of Sp1 expression, W/D of lung tissue, myeloperoxidase activities, and higher levels of interleukin(IL)-6, tumor necrosis factor (TNF)-α and IL-1β, cell apoptosis rate and Notch-1, and Hes-1, nuclear factor (NF)-κB P65 expressions in lung tissue. Compared with model mice, mice in the si-Sp1 group and the miR-133b mimic group had significantly lower W/D of lung tissue, myeloperoxidase activities, lower levels of IL-6, TNF-α and IL-1β, cell apoptosis rate and Notch-1, Hes-1, and NF-κB P65 expressions in lung tissue. Mice treated by miR-133b inhibitor showed opposite results in all above parameters, which were similar with those in the model group. The negative effects of miR-133b inhibitor could be reversed by the combination use of si-Sp1.
Conclusion: Overexpression of miR-133b could inhibit Sp1 expression, thereby improving severe acute pancreatitis in rats and playing a protective role in acute lung injury.
Keywords: acute lung injury; acute pancreatitis; miR-133b.
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