The JAK2/STAT3 signaling pathway is required for inflammation and cell death induced by cerulein in AR42J cells

W.-D. Chen, J.-L. Zhang, X.-Y. Wang, Z.-W. Hu, Y.-B. Qian

Department of Emergency Surgery, The 1st Affiliated Hospital of Anhui Medical University, Hefei, China. 1738884943@qq.com

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• Pharmacology

OBJECTIVE: The study was designed to investigate the JAK2/STAT3 signaling pathway in pancreatitis and its association with inflammation and cell death to provide a potential treatment method for pancreatitis.

MATERIALS AND METHODS: The rat pancreatic acinar AR42J cells were used for the study, and they were transfected with JAK2 and STAT3 siRNAs to mimic knockdown condition. Cerulein was used to treat AR42J cells. Western blot and ELISA were employed to detect the expression of related proteins. Flow cytometry was done to analysis the necrosis of AR42J cells.

RESULTS: In this study, we found that cell death and the secretion of IL-6 and TGF-β1 were significantly increased, and the JAK2/STAT3 signaling pathway was activated in cerulein-induced AP. To determine the role of JAK2 and STAT3, JAK2 siRNA and STAT3 siRNA were used to block JAK2 and STAT3, respectively. The levels of IL-6 and TGF-β1 levels in the medium were lower in JAK2 siRNA and STAT3 siRNA-treated cells compared with controls. Flow cytometry analysis showed that the level of cell death, expression of cleaved caspase-3, and the release of LDH were decreased following JAK2 siRNA and STAT3 siRNA treatment.

CONCLUSIONS: These findings point to a novel role for the JAK2/STAT3 signaling pathway in the progression of cerulein-induced AP.

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