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Updated: Jan 28, 2026

Saturated Fatty Acids Induce Ceramide-associated Macrophage Cell Death
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Published on: October 31, 2017

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

W-D Chen1, J-L Zhang, X-Y Wang

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

European Review for Medical and Pharmacological Sciences
|March 7, 2019
PubMed
Abstract

Insights

The Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) pathway is activated in pancreatitis, promoting inflammation and cell death. Inhibiting this pathway may offer a new treatment strategy for acute pancreatitis (AP).

Area of Science:

  • Cellular and Molecular Biology
  • Gastroenterology
  • Immunology

Background:

  • Pancreatitis is a significant gastrointestinal disease characterized by inflammation and acinar cell death.
  • The Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) signaling pathway plays a role in various cellular processes, including inflammation and survival.

Purpose of the Study:

  • To investigate the role of the JAK2/STAT3 signaling pathway in cerulein-induced acute pancreatitis (AP).
  • To explore the association between JAK2/STAT3 activation, inflammation, and cell death in AP.
  • To evaluate the potential of targeting JAK2/STAT3 as a therapeutic strategy for pancreatitis.

Main Methods:

  • Rat pancreatic acinar AR42J cells were treated with cerulein to induce AP.
  • JAK2 and STAT3 were knocked down using small interfering RNA (siRNA).
  • Western blot, ELISA, and flow cytometry were used to assess protein expression, cytokine secretion (IL-6, TGF-β1), cell death, cleaved caspase-3, and lactate dehydrogenase (LDH) release.

Main Results:

  • Cerulein-induced AP activated the JAK2/STAT3 pathway, increasing cell death and secretion of IL-6 and TGF-β1.
  • JAK2 or STAT3 knockdown significantly reduced IL-6 and TGF-β1 levels.
  • Inhibition of JAK2/STAT3 decreased cell death, cleaved caspase-3 expression, and LDH release.

Conclusions:

  • The JAK2/STAT3 signaling pathway is critically involved in the pathogenesis of cerulein-induced AP.
  • Targeting the JAK2/STAT3 pathway demonstrates therapeutic potential for managing pancreatitis by reducing inflammation and cell death.

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