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B activation is associated with hormone-induced
pancreatitis
Departments of 1 Medicine and 2 Surgery, Veterans Affairs Medical Center, West Los Angeles and University of California, Los Angeles, California 90073
Inflammation and cell death are critical to
pathogenesis of acute pancreatitis. Here we show that transcription
factor nuclear factor-
B (NF-B), which regulates these processes,
is activated and plays a role in rat cerulein pancreatitis. NF-B was
strongly activated in the pancreas within 30 min of cerulein infusion; a second phase of NF-B activation was prominent at 3-6 h. This biphasic kinetics could result from observed transient degradation of
the inhibitory protein IB
and slower but sustained degradation of
IB
. The hormone also caused NF-B translocation and IB
degradation in vitro in dispersed pancreatic acini. Both p65/p50 and
p50/p50, but not c-Rel, NF-B complexes were manifest in pancreatitis
and in isolated acini. Coinfusion of CCK JMV-180, which abolishes pancreatitis, prevented cerulein-induced NF-B activation. The second
but not early phase of NF-B activation was inhibited by a
neutralizing tumor necrosis factor- antibody. Antioxidant
N-acetylcysteine (NAC) blocked NF-B
activation and significantly improved parameters of pancreatitis. In
particular, NAC inhibited intrapancreatic trypsin activation and mRNA
expression of cytokines interleukin-6 and KC, which were dramatically
induced by cerulein. The results suggest that NF-B activation is an
important early event that may contribute to inflammatory and cell
death responses in acute pancreatitis.
pancreatic acinar cell; interleukin-6; KC; IB
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