Different cell death modes of pancreatic acinar cells on macrophage activation in rats

Background The pathogenesis of acute pancreatitis is complex and largely unclear. The aim of this study was to explore the relationship between modes of cell death in pancreatic acinar cells, the release of cell contents and the inflammatory response of macrophages. Methods Our experiment included f...

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Veröffentlicht in:Chinese medical journal 2008-10, Vol.121 (19), p.1920-1924
Hauptverfasser: Liang, Tao, Liu, Tie-fu, Xue, Dong-bo, Sun, Bei, Shi, Li-jun
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Sprache:eng
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Zusammenfassung:Background The pathogenesis of acute pancreatitis is complex and largely unclear. The aim of this study was to explore the relationship between modes of cell death in pancreatic acinar cells, the release of cell contents and the inflammatory response of macrophages. Methods Our experiment included four groups: group A (the control group), group B (AR42J cells overstimulated by caerulein), group C (AR42J cells treated with lipopolysaccharide and caerulein), and group D (AR42J cells treated with octreotide and caerulein). Apoptosis and oncosis, and the release of amylase and lactate dehydrogenase (LDH) from AR42J cells were detected. Rat macrophages were stimulated by 1 ml supernatant of culture medium of AR42J cells. Finally, NF-KB activation and TNF-a and IL-113 secretion by macrophages were detected. Results Oncotic cells in group C increased while apoptotic cells decreased (P 〈0.05); cells in group D had the inverse reaction. The release of amylase and LDH changed directly with the occurrence of oncosis. The transcription factor NF-KB was activated and secretion of TNF-α and IL-1β were significantly higher in group C than in group B (P 〈0.05); in group D, these actions were significantly lower than in group B (P〈0.05). This trend was in line with changes in amylase and LDH production. Conclusion There is a close relationship between modes of pancreatic acinar cell death, the release of cell contents and the inflammatory reaction of macrophages.
ISSN:0366-6999
2542-5641
DOI:10.1097/00029330-200810010-00013