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p38 MAPK inhibition alleviates experimental acute pancreatitis in mice

Ming-Hua Cao1, Jing Xu, Hai-Dong Cai

  • 1Department of Pathophysiology, Institute of Digestive Disease, Tongji University School of Medicine, Shanghai 200092, China. liyongyu@tongji.edu.cn.

Hepatobiliary & Pancreatic Diseases International : HBPD INT
|February 7, 2015
PubMed
Abstract

Insights

The p38 mitogen-activated protein kinase (MAPK) pathway regulates inflammation and heat shock protein (HSP) expression in acute pancreatitis. Inhibiting p38 MAPK reduces pancreatitis severity and associated inflammatory markers in mice.

Area of Science:

  • Molecular Biology
  • Immunology
  • Gastroenterology

Background:

  • Mitogen-activated protein kinases (MAPKs) signaling pathways are implicated in inflammatory processes.
  • The precise role of p38 MAPK in acute pancreatitis remains unclear.

Purpose of the Study:

  • To investigate the role of p38 MAPK in the pathogenesis of acute pancreatitis in a mouse model.
  • To evaluate the effects of p38 MAPK inhibition on inflammatory markers and heat shock protein expression.

Main Methods:

  • Acute pancreatitis was induced in mice using repeated cerulein injections.
  • Mice were treated with either saline or the p38 MAPK inhibitor SB203580.
  • Pancreatic histology, enzyme levels, cytokine profiles, myeloperoxidase activity, and protein expression (p38 MAPK, HSP60, HSP70) were assessed.

Main Results:

  • Cerulein-induced pancreatitis led to p38 MAPK activation and overexpression of HSP60 and HSP70 in pancreatic tissues.
  • SB203580 treatment significantly inhibited p38 MAPK activation.
  • Inhibition of p38 MAPK reduced HSP60/HSP70 expression, serum inflammatory cytokines, and lung myeloperoxidase activity.

Conclusions:

  • The p38 MAPK signaling pathway plays a critical role in regulating inflammatory responses during acute pancreatitis.
  • p38 MAPK influences the expression of HSP60 and HSP70 in the context of acute pancreatitis.

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