Effects of c-Jun N-terminal kinase signaling pathway on severe acute pancreatitis-associated lung injury.

Abstract

OBJECTIVE:

The objective of this study was to investigate the effects of the c-Jun N-terminal kinase (JNK) signaling pathway on rats' acute pancreatitis-associated lung injury (APALI).

METHODS:

Seventy-two Sprague-Dawley rats were randomly divided into 3 groups, namely, the sham operation (SO) group, the severe acute pancreatitis (SAP) group, and the SP600125 group. The SAP model was established by injection of 5% sodium taurocholate into the pancreatic duct. The samples were taken at 3, 6, 12, and 24 hours. Serum amylase, pathologic lesions of the pancreas and lung tissues, wet-to-dry weight ratio of the lung, myeloperoxidase (MPO) activity of the lung, tumor necrosis factor α (TNF-α), interleukin 1β (IL-1β), intercellular adhesion molecule 1 (ICAM-1), and p-JNK of lung tissues were detected.

RESULTS:

The wet-to-dry weight ratio, MPO activity, and IL-1β, TNF-α, ICAM-1, and p-JNK levels in the SAP group significantly increased compared with those in the SO group. The scores of lung pathologic injury significantly increased, consistent with the APALI. The wet-to-dry weight ratio, MPO activity, IL-1β, TNF-α, ICAM-1, p-JNK expressions, and lung pathologic injury scores in the SP600125 group decreased compared with those in the SAP group. p-JNK was closely correlated with MPO activity, IL-1β, ICAM-1, and total scores of lung injury.

CONCLUSIONS:

The JNK signaling pathway plays a critical role in APALI. On the other hand, application of a specific JNK inhibitor can contribute to alleviation of APALI.

• Authors: Mingdong Liu, Liangliang Shi, Min Chen, Suyu Chen, Xiaoping Zou
• Journal: Pancreas (Pancreas) Vol. 41 Issue 3 Pg. 358-66 (Apr 2012) ISSN: 1536-4828 [Electronic] United States
• PMID: 22015972 (Publication Type: Journal Article)

Chemical References

• Anthracenes
• Interleukin-1
• Protein Kinase Inhibitors
• Tumor Necrosis Factor-alpha
• Intercellular Adhesion Molecule-1
• pyrazolanthrone
• Taurocholic Acid
• Peroxidase
• JNK Mitogen-Activated Protein Kinases
• Amylases

Topics

• Acute Disease
• Amylases (blood)
• Animals
• Anthracenes (pharmacology)
• Disease Models, Animal
• Intercellular Adhesion Molecule-1 (metabolism)
• Interleukin-1 (metabolism)
• JNK Mitogen-Activated Protein Kinases (antagonists & inhibitors, metabolism)
• Lung (drug effects, enzymology, pathology)
• Lung Injury (enzymology, etiology, pathology, prevention & control)
• Male
• Pancreas (drug effects, enzymology, pathology)
• Pancreatitis (chemically induced, complications, drug therapy, enzymology, pathology)
• Peroxidase (metabolism)
• Phosphorylation
• Protein Kinase Inhibitors (pharmacology)
• Rats
• Rats, Sprague-Dawley
• Signal Transduction (drug effects)
• Taurocholic Acid
• Time Factors
• Tumor Necrosis Factor-alpha (metabolism)