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Research Center for Alcoholic Liver and Pancreatic Diseases and Department of Medicine, University of California, Los Angeles and Veterans Affairs Greater Los Angeles Healthcare System, Los Angeles, California 90073
Treatments for pancreatitis are
limited. Activation of transcription factor NF-
B, a key regulator of
inflammatory molecule expression, is an early event in experimental
pancreatitis and correlates with the inflammatory response. We report
here that curcumin, a natural phytochemical known to inhibit NF-B
and activator protein (AP)-1, another important proinflammatory
transcription factor, ameliorates pancreatitis in two rat models. In
both cerulein pancreatitis and pancreatitis induced by a combination of
ethanol diet and low-dose CCK, curcumin improved the severity of the
disease as measured by a number of parameters (histology, serum
amylase, pancreatic trypsin, and neutrophil infiltration). Curcumin
markedly inhibited NF-B and AP-1 activation, assessed by DNA binding
and degradation of inhibitory IB proteins, and the induction of
mRNAs for cytokines IL-6 and TNF-
, the chemokine KC, and inducible nitric oxide synthase in pancreas. Curcumin also blocked
CCK-induced NF-B and AP-1 activation in isolated pancreatic acini.
Our findings indicate that blocking key signals of the inflammatory
response ameliorates pancreatitis in both ethanol and nonethanol
models. They suggest that curcumin, which is currently in clinical
trials for cancer prevention, may be useful for treatment of pancreatitis.
nuclear factor-B; activator protein-1; cerulein; cholecystokinin; chemokines; N-acetylcysteine
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