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Our results support the hypothesis that COX-2 may be involved in inflammatory responses in chronic pancreatitis and in the progression of this chronic inflammatory disease.

Taken together, our results show enhanced GSH levels in pancreatic carcinoma and an essential role of GSH in cell proliferation and in resistance of AsPC-1 cells. Therefore, GSH-depletion may improve the efficacy of adjuvant therapy in pancreatic carcinoma.

Caspase-1 (interleukin-1L L-converting enzyme) is reported to play an important role in the regulation of apoptosis. We investigated the inhibition of caspase-1 by the cell permeable caspase-1 inhibitor Ac-AAVALLPAVLLALLAP-YVAD.CHO in pancreatic carcinoma cells. Inhibition of caspase-1 induced a non-apoptotic/`necrotic-like' cell death in AsPC-1, BxPC-3, MiaPaCa-2 and Panc-1 cells. Expression levels of bcl-2 and bax were up-regulated in caspase-1 inhibitor-treated cells while that of bcl-x L remained unaltered. Our observations support our previous findings that caspase-1 is potentially involved in antiapoptotic processes in pancreatic carcinoma. ß

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