Objective: To study the role of Janus kinase/signal transducer and activator of transcription 3 (JAK/STAT3) in injury of alveolar type II epithelial cells (AT II) in severe acute pancreatitis (SAP).
Methods: The rat model of SAP was reproduced intraductal injection of sodium taurocholate. Serum was collected for examinations. AT II cells in primary culture were randomized to be treated with serum from rats with SAP (SAP group), or SAP serum+AG490 (JAK inhibitor, SAP+AG490 group), while the normal cell control was cultured with Dulbecco improved Eagle medium (DMEM). AT II cells were collected after the treatment to determine the activation of STAT3 by electrophoretic mobility shift assay (EMSA), STAT3 mRNA expression by reverse transcription-polymerase chain reaction (RT-PCR), STAT3 protein expression by Western blotting, surfactant protein C (SP-C) level in AT II and apoptosis of AT II with flow cytometry.
Results: Compared with control group, activation of STAT3 was enhanced in SAP group, and expression of STAT3 mRNA and protein was also enhanced, level of SP-C protein declined (2 hours SP-C fluorescence index 0.69+/-0.02 vs. 1.02+/-0.03, P<0.01), and apoptosis of AT II increased [(11.55+/-1.10)% vs. (5.30+/-0.36)%, P<0.05]. Compared with SAP group, activation of STAT3 was attenuated in SAP+AG490 group, expression of STAT3 mRNA and protein was lowered, and level of SP-C protein declined (2 hours SP-C fluorescence index 0.48+/-0.10 vs. 0.69+/-0.02, P<0.01), and the apoptosis of AT II increased [(13.92+/-0.82)% vs. (11.55+/-1.10)%, P<0.05].
Conclusion: The results suggest that JAK/STAT3 pathway might be involved in the pathogenesis of injury to AT II in SAP.